Cardio T1-11 Flashcards
1
Q
- How does the American Heart Association define hypertension?
A
Hypertension is defined as persistent blood pressure of ≥130/80 mmHg. If only one is high, it is considered isolated systolic or diastolic hypertension.
2
Q
How does the JNC 81 define hypertension?
A
The JNC 81 defines hypertension as persistent blood pressure of ≥140/90 mmHg.
3
Q
What is the most common risk factor for hypertension?
A
The most common risk factor for hypertension is cardiovascular disease.
4
Q
How is hypertension classified?
A
Hypertension is divided into primary (essential) hypertension and secondary hypertension based on the underlying cause.
5
Q
What percentage of adult hypertension cases are due to primary hypertension?
A
About 95% of hypertension cases in adults are due to primary hypertension.
6
Q
What percentage of children’s hypertension cases are due to primary hypertension?
A
About 20% of hypertension cases in children are due to primary hypertension.
7
Q
What are some non-modifiable risk factors for primary hypertension?
A
Non-modifiable risk factors include a positive family history, ethnicity, and advanced age.
8
Q
What are some modifiable risk factors for primary hypertension?
A
Modifiable risk factors include obesity, diabetes, smoking, a diet high in sodium or low in potassium, physical inactivity, and psychological stress.
9
Q
What is considered optimal (normal) blood pressure?
A
Optimal blood pressure lies between 90/60 mmHg and 120/80 mmHg.
10
Q
What is considered hypotension and hypertension based on blood pressure?
A
Blood pressure below 90/60 mmHg is considered hypotension, and above 120/80 mmHg is considered hypertension.
11
Q
How are the grades (or stages) of hypertension defined?
A
The stages of hypertension are determined based on blood pressure levels, but specific stages were not detailed in this text.
12
Q
A
13
Q
What are the clinical features of primary hypertension?
A
Primary hypertension is usually asymptomatic until end-organ damage or a hypertensive crisis occurs.
14
Q
What symptoms may accompany secondary hypertension?
A
Symptoms of secondary hypertension align with the underlying cause.
15
Q
What are some nonspecific symptoms that may be associated with hypertension?
A
Nonspecific symptoms can include headaches (especially in the morning), dizziness, tinnitus, blurred vision, nervousness, fatigue, sleep disturbances, and chest discomfort.
16
Q
How is primary hypertension diagnosed?
A
Primary hypertension is diagnosed over three separate office visits, with at least three blood pressure measurements taken per visit.
17
Q
Describe the process of measuring blood pressure manually using the auscultatory method.
A
The patient rests in a seated position for at least 5 minutes. A blood pressure cuff is applied to the arm above the brachial artery, the cuff is inflated 30 mmHg above expected systolic pressure, and the stethoscope is placed over the brachial artery.
The cuff is deflated, and systolic pressure is noted when the pulse is first heard, and diastolic pressure is noted when the pulse disappears.
18
Q
What factors should be avoided before taking a blood pressure measurement?
A
Caffeine intake, drug use, and smoking should be avoided before a blood pressure measurement.
19
Q
What is White Coat Syndrome and masked hypertension?
A
White Coat Syndrome refers to higher blood pressure readings in a clinical setting due to anxiety, while masked hypertension is when blood pressure is normal in the clinic but elevated in everyday life.
20
Q
What is Home Blood Pressure Monitoring (HBPM) and how can it benefit patients?
A
HBPM allows patients to take their own BP readings at home, helping avoid White Coat Syndrome. Studies show home readings can be about 30 mmHg lower than office readings. It is also more cost-effective than ambulatory BP monitoring.
21
Q
What is Ambulatory Blood Pressure Monitoring (ABPM) and how does it work?
A
ABPM involves wearing a device that measures blood pressure every 30 minutes during the day and hourly at night for 24 hours, providing a comprehensive picture of the patient’s overall blood pressure.
22
Q
What is a hypertensive crisis, and how is it defined?
A
A hypertensive crisis is an acute increase in blood pressure (>180/120 mmHg) that can cause or worsen end-organ damage. It is further subdivided into hypertensive urgency and hypertensive emergency.
23
Q
A
24
Q
What is aortic stenosis (AS)?
A
Aortic stenosis is a valvular heart disease characterized by the narrowing of the aortic valve, reducing the normal orifice size from about 4 cm² to less than 1 cm² in severe cases, obstructing blood flow from the left ventricle into the aorta.
25
What are the consequences of aortic stenosis on the left ventricle?
Aortic stenosis leads to chronic and progressive excess load on the left ventricle, potentially resulting in left ventricular failure.
26
What are the common symptoms of aortic stenosis when it becomes symptomatic?
Common symptoms of symptomatic aortic stenosis include syncope, angina pectoris, and dyspnea upon exertion.
27
What is a key finding during auscultation in a patient with aortic stenosis?
Auscultation reveals a harsh, crescendo-decrescendo systolic murmur that radiates to the carotids, and there are delayed and diminished carotid upstrokes.
28
What is the gold standard for diagnosing aortic stenosis?
Echocardiography is the noninvasive gold standard for diagnosing aortic stenosis.
29
How is mild asymptomatic aortic stenosis managed?
Mild asymptomatic aortic stenosis is managed conservatively with monitoring and medical treatment of related conditions such as hypertension.
30
What is the definitive treatment for symptomatic or severe aortic stenosis?
The definitive treatment for symptomatic or severe aortic stenosis is aortic valve replacement (AVR), either through surgical AVR or transcatheter AVR (TAVR) for high-risk patients.
31
What acute complications are patients with severe aortic stenosis at risk for?
Patients with severe aortic stenosis are at high risk for acute complications such as heart failure and cardiogenic shock, requiring critical care and expedited surgery or TAVR.
32
What is the most common valvular heart disease in industrialized countries?
Aortic stenosis is the most common valvular heart disease in industrialized countries.
33
What are the most common causes of aortic stenosis?
The most common causes of aortic stenosis are:
Aortic valve sclerosis (calcification and fibrosis of the leaflets), which is prevalent in older patients.
Bicuspid aortic valve, which predisposes the valve to calcification.
Rheumatic fever (less common, often affects the mitral valve).
Endocarditis (least common cause).
34
What condition related to aging is the most common cause of aortic stenosis?
Aortic valve sclerosis, the calcification and fibrosis of the leaflets, is the most common cause of aortic stenosis and increases in prevalence with age (35% of patients over 80).
35
How does a bicuspid aortic valve contribute to aortic stenosis?
A bicuspid aortic valve, caused by the fusion of two leaflets in utero, predisposes the valve to dystrophic calcification, leading to aortic stenosis.
36
What is the pathophysiology of aortic stenosis?
A narrowed aortic valve opening during systole obstructs blood flow from the left ventricle, increasing LV pressure, leading to left ventricular concentric hypertrophy, which results in increased LV oxygen demand and impaired ventricular filling during diastole, causing left heart failure.
37
What are the three major symptoms (SAD) associated with severe aortic stenosis?
The three major symptoms (SAD) of severe aortic stenosis are syncope, angina pectoris, and dyspnea.
38
What are some physical exam findings in aortic stenosis?
Physical exam findings include small BP amplitude, decreased pulse pressure, and a weak and delayed distal pulse known as "pulsus parvus et tardus."
39
What is a key auscultation finding in aortic stenosis?
A harsh crescendo-decrescendo systolic murmur best heard in the 2nd right intercostal space, which may also radiate to the carotids, is a key auscultation finding in aortic stenosis.
40
What characterizes severe aortic stenosis during auscultation?
Severe aortic stenosis is characterized by a soft S2 sound and may also have an early systolic ejection click.
41
What is the preferred method for diagnosing aortic stenosis?
Echocardiography is the preferred method for diagnosing aortic stenosis, assessing LV function, wall thickness, valve area, and transvalvular systolic gradient.
42
What are the two types of echocardiography used to diagnose aortic stenosis?
Transthoracic echocardiography (TTE) is the primary noninvasive test, while transesophageal echocardiography (TEE) is used for confirmation of TTE findings.
43
Is there any medical therapy that improves outcomes in aortic stenosis?
No medical therapy can improve the outcome of aortic stenosis, though coexisting hypertension should be treated and sinus rhythm should be maintained.
44
What are the indications for intervention in aortic stenosis?
Intervention is indicated in symptomatic patients with severe, high-gradient aortic stenosis (mean gradient ≥40 mmHg) and asymptomatic patients with severe AS and reduced LVEF (<50%).
45
When is surgical aortic valve replacement (AVR) recommended?
Surgical aortic valve replacement is recommended for patients with low surgical risk.
46
When is transcatheter aortic valve replacement (TAVR) recommended?
TAVR is recommended for patients unsuitable for surgery or those with high surgical risk.
47
What is transcatheter aortic valve replacement (TAVR), and when is it performed?
TAVR is a procedure for high-risk surgical patients with severe aortic stenosis and a predicted survival of over 12 months. It can be performed via transfemoral, transaortic, or transapical routes.
48
What is percutaneous balloon valvuloplasty, and who is it used for?
Percutaneous balloon valvuloplasty is used in younger patients without aortic valve calcification to relieve aortic stenosis.
49
2. What is ischemic heart disease (IHD) and its most common cause?
Ischemic heart disease (also known as coronary artery disease) is most commonly caused by atherosclerosis, which leads to a reduced blood supply to the myocardium, causing a mismatch between oxygen supply and demand.
50
What is the cardinal symptom of ischemic heart disease?
The cardinal symptom of ischemic heart disease is acute retrosternal chest pain, also known as angina.
51
What are other common symptoms of ischemic heart disease besides angina?
Other common symptoms include dyspnea, dizziness, anxiety, and nausea.
52
What can severe myocardial ischemia lead to?
Severe myocardial ischemia can lead to myocardial infarction (MI).
53
How is ischemic heart disease diagnosed?
Ischemic heart disease is diagnosed using a cardiac stress test and/or coronary catheterization.
54
What are the main components of ischemic heart disease management?
Management includes primary and secondary prevention of atherosclerosis, antianginal treatment, and, in severe cases, revascularization.
55
How is ischemic heart disease subdivided?
Ischemic heart disease is subdivided into Chronic (Stable) Coronary Syndrome and Acute Coronary Syndrome.
56
What are INOCA and MINOCA in the context of ischemic heart disease?
INOCA refers to ischemia with no obstructive coronary artery disease, while MINOCA refers to myocardial infarction with nonobstructive coronary arteries.
57
What are the main risk factors for ischemic heart disease?
The main risk factors include diabetes mellitus, family history, smoking, hyperlipidemia, obesity, hypertension, and age.
58
What is the leading cause of death worldwide, and what is its most common underlying cause?
Coronary artery disease (CAD) is the leading cause of death worldwide, with atherosclerosis being the most common underlying cause.
59
What are the possible clinical manifestations of ischemic heart disease?
The clinical manifestations include asymptomatic cases (less than 70% stenosis), angina (stable or unstable), myocardial infarction (MI), and sudden cardiac death.
60
What is the first step in diagnosing ischemic heart disease?
The first step is taking the patient's history and conducting a physical examination.
61
What is the best initial test for all types of chest pain?
A resting ECG is the best initial test for all types of chest pain.
62
What ECG findings may indicate a previous MI or unstable angina?
ST-segment depression or T-wave inversion/flattening may indicate a previous MI or unstable angina.
63
What is the test of choice for diagnosing stable ischemic heart disease?
A cardiac exercise stress test is the test of choice for diagnosing stable ischemic heart disease.
64
When is a cardiac pharmacological stress test performed?
It is performed when a patient cannot exercise or has contraindications for exercising, using agents like dobutamine.
65
What is the gold standard for diagnosing coronary artery disease (CAD)?
Cardiac catheterization is the gold standard for diagnosing CAD.
66
What is Holter monitoring used for in ischemic heart disease?
Holter monitoring is used to detect silent ischemia.
67
What do elevated heart enzymes such as troponin, creatine kinase, and myoglobin indicate?
Elevated heart enzymes in the blood indicate heart damage, such as from a myocardial infarction (MI).
68
What does coronary angiography involve, and what does it diagnose?
Coronary angiography involves injecting dye into the heart's blood vessels and taking X-ray images to diagnose blockages in coronary arteries.
69
How are cardiac CT and MRI used in diagnosing coronary artery disease?
Cardiac CT and MRI provide detailed images of the heart and blood vessels, showing artery narrowing or heart enlargement.
70
What are the general treatment approaches for coronary artery disease?
All patients should reduce risk factors and start on antiplatelet drugs. Mild CAD is treated with pharmacologic therapy, moderate CAD may require coronary angiography and PCI, and severe CAD may need revascularization or coronary artery bypass grafting (CABG).
71
What is the first-line antianginal treatment for ischemic heart disease?
First-line antianginal treatment includes β-blockers and nitrates.
72
What are second-line antianginal medications?
Second-line antianginal medications include calcium channel blockers (CCBs) and ranolazine.
73
What are the two types of revascularization procedures for treating CAD?
The two types of revascularization procedures are percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG).
74
75
What is cardiac rehabilitation, and what is its main goal?
Cardiac rehabilitation is a comprehensive exercise, education, and behavior modification program aimed at helping patients restore and maintain optimal health while reducing the risk of future heart problems.
76
Who can benefit from cardiac rehabilitation programs?
People recovering from heart attacks, heart surgery, or percutaneous coronary intervention (PCI) procedures, such as stenting and angioplasty, can benefit from cardiac rehabilitation programs.
77
What are the main components of a cardiac rehabilitation program?
Components include medical evaluation, physical activity program, counseling and education, lifestyle modification, and support for returning to normal activities and work.
78
What is the purpose of the medical evaluation in cardiac rehabilitation?
The medical evaluation helps assess the patient's needs and limitations, allowing the medical staff to tailor a rehabilitation program and set appropriate goals.
79
How is physical activity managed in cardiac rehabilitation programs?
Physical activity is tailored to the patient’s needs, and heart rate and blood pressure are monitored during exercise to ensure safety.
80
What types of lifestyle education are typically included in cardiac rehabilitation?
Lifestyle education includes counseling on understanding and managing the heart condition, dietary planning with a dietitian, smoking cessation, and stress management.
81
How long do most cardiac rehabilitation programs last?
Most cardiac rehabilitation programs last about three months, though some patients may follow the program longer or participate in an intensive program lasting one to two weeks.
82
Who are the members of the cardiac rehabilitation team?
The cardiac rehabilitation team includes cardiologists, nurses, dietitians, physical therapists, and mental health specialists.
83
In what settings can cardiac rehabilitation be performed?
Cardiac rehabilitation can be done as an inpatient program or an outpatient program, depending on the reason for therapy initiation.
84
What therapies are included in cardiac rehabilitation?
Therapies include nutritional therapy, weight loss programs, management of lipid abnormalities, blood pressure control, diabetes management, stress management, and smoking cessation.
85
What are the benefits of exercise-based programs in cardiac rehabilitation?
Exercise-based programs improve cardiac fitness, microvascular circulation, quality of life, and reduce readmission rates.
86
3. What is heart failure (CHF) and its main causes?
Heart failure, or congestive heart failure (CHF), is a condition where the heart can't pump enough blood to meet the body's needs due to pathological changes in the myocardium. The three main causes are coronary artery disease (CAD), hypertension, and diabetes mellitus.
87
What are the two types of ventricular dysfunction in heart failure?
The two types are systolic dysfunction (HFrEF) and diastolic dysfunction (HFpEF). Systolic dysfunction is characterized by the heart's inability to pump effectively, while diastolic dysfunction is related to impaired filling of the heart.
88
What are the common causes of systolic and diastolic dysfunction in heart failure?
Systolic dysfunction (HFrEF): CAD, MI, hypertension, valvular heart disease, diabetic cardiomyopathy, dilated cardiomyopathy, arrhythmias, myocarditis.
Diastolic dysfunction (HFpEF): Restrictive cardiomyopathy, hypertrophic cardiomyopathy, pericardial tamponade, constrictive pericarditis.
89
What are the clinical features of left-sided heart failure (LHF) and right-sided heart failure (RHF)?
LHF: Leads to pulmonary edema causing dyspnea (shortness of breath).
RHF: Leads to systemic venous congestion, causing pitting edema, jugular venous distention, and hepatomegaly.
90
What is biventricular (global) CHF, and how does it manifest?
Biventricular CHF involves both left and right heart failure, presenting with symptoms of both types, such as pulmonary edema, systemic venous congestion, fatigue, tachycardia, and nocturia.
91
What is the difference between systolic and diastolic dysfunction in terms of ejection fraction?
Systolic dysfunction (HFrEF): Increased EDV, reduced stroke volume, and ejection fraction (EF).
Diastolic dysfunction (HFpEF): Reduced stroke volume and EDV but preserved ejection fraction (EF). Normal EF is between 50%-70%.
92
How is congestive heart failure (CHF) diagnosed?
CHF is diagnosed based on clinical presentation and tests like brain natriuretic peptide (BNP) levels, chest X-ray, and ECG to assess severity and determine the underlying causes.
93
What is the main treatment approach for congestive heart failure (CHF)?
Treatment involves lifestyle modifications, managing underlying conditions (e.g., hypertension), comorbidities (e.g., anemia), and using pharmacologic agents to reduce the heart's workload.
94
What are the hallmark symptoms of right-sided heart failure (RHF)?
Symptoms of RHF include pitting edema, jugular venous distension, and hepatomegaly, and it may lead to Cor pulmonale if caused by a respiratory system disorder.
95
What is high-output CHF, and what causes it?
High-output CHF is a rare form of heart failure caused by conditions that increase cardiac output, overwhelming the heart's capacity to pump efficiently.
96
97
What is hypertrophic cardiomyopathy, and how does it affect the heart?
Hypertrophic cardiomyopathy occurs when the cardiac muscle wall enlarges, crowding the ventricular space, which reduces the room for ventricular filling.
98
What is restrictive cardiomyopathy, and how does it impact heart function?
Restrictive cardiomyopathy is when the cardiac muscle wall becomes stiff and less compliant, preventing the heart from filling properly during diastole.
99
What are some risk factors for congestive heart failure (CHF)?
Risk factors for CHF include obesity, smoking, COPD, and drug/alcohol abuse.
100
What is the Frank-Starling mechanism, and how is it affected in heart failure?
The Frank-Starling mechanism normally regulates contractility by increasing preload, but in CHF, this compensatory mechanism fails, leading to impaired cardiac output.
101
What are the consequences of systolic and diastolic dysfunction in heart failure?
Systolic dysfunction: Reduced cardiac output leading to poor organ perfusion, potentially causing organ dysfunction (e.g., renal failure, hypotension).
Diastolic dysfunction: Increased LV volume and pressure, leading to pulmonary congestion, edema, and organ congestion.
102
What is "nutmeg liver," and what causes it?
"Nutmeg liver" is the macroscopic appearance of the liver, resembling a nutmeg seed, caused by ischemia and fatty degeneration due to hepatic venous congestion in heart failure.
103
What are the main clinical symptoms of left-sided heart failure?
Symptoms of left-sided heart failure include dyspnea (shortness of breath), orthopnea, paroxysmal nocturnal dyspnea, and pulmonary congestion (e.g., crackles/rales at lung bases).
104
What are the key signs of right-sided heart failure?
Signs of right-sided heart failure include peripheral pitting edema, jugular vein distention, nocturia, hepatomegaly, ascites, and Kussmaul sign (jugular vein distention during inspiration).
105
What are the NYHA (New York Heart Association) stages of heart failure?
Class I: Symptoms only occur with vigorous activity, nearly asymptomatic.
Class II: Symptoms with moderate exertion, slight limitation of activity, comfortable at rest.
Class III: Symptoms with daily activities, marked limitation, comfortable only at rest.
Class IV: Symptoms at rest, incapacitating.
106
What diagnostic tools are used to assess heart failure?
Transthoracic echocardiogram: Gold standard to assess systolic and diastolic function.
Chest X-ray: Shows cardiomegaly (boot-shaped heart) and pulmonary congestion.
Lab tests: Elevated BNP, NT-pro BNP, and ANP levels.
107
108
What is secondary hypertension (HTN), and how common is it in adults and children?
Secondary HTN is hypertension caused by an identifiable underlying condition. It accounts for 5-15% of cases in adults and 70-85% of cases in children under 12 years old.
109
What are the age groups typically associated with the onset of secondary hypertension?
Secondary hypertension typically occurs in people younger than 25 years old or older than 55 years old.
110
What does the pneumonic "RECENT" stand for in causes of secondary hypertension?
R: Renal (e.g., renal artery stenosis, SLE, tumors)
E: Endocrine (e.g., Cushing syndrome, Conn syndrome, hyperthyroidism)
C: Coarctation of the aorta
E: Estrogen (oral contraceptives)
N: Neurologic (e.g., increased intracranial pressure)
T: Treatment (e.g., NSAIDs, corticosteroids)
111
What are some renal causes of secondary hypertension?
Renal causes of secondary hypertension include renal artery stenosis, systemic lupus erythematosus (SLE), tumors, autosomal dominant polycystic kidney disease (ADPKD), and renal failure.
112
Name a few endocrine causes of secondary hypertension.
Endocrine causes include Cushing syndrome, Conn syndrome (primary hyperaldosteronism), and hyperthyroidism.
113
What medications can lead to secondary hypertension?
Medications that can cause secondary hypertension include NSAIDs, sympathomimetic drugs, and corticosteroids.
114
What general indicators suggest secondary hypertension?
General indicators of secondary hypertension include young age, abrupt onset, disproportionate end-organ damage, recurrent hypertensive crises, and resistant hypertension.
115
What diagnostic tests are used to determine the underlying cause of secondary hypertension?
Diagnostic tests may include urinalysis, complete blood count (CBC), blood chemistry profile, and imaging modalities like ultrasound of the kidney and its vessels.
116
What is the primary approach to treating secondary hypertension?
The primary treatment for secondary hypertension is managing the underlying cause, such as using medications or surgery (e.g., removing a tumor). Once the condition is controlled, hypertension often normalizes.
117
What should be done if hypertension persists after treating the underlying cause of secondary hypertension?
If hypertension remains elevated after addressing the underlying condition, both pharmacological (medications) and nonpharmacological measures (lifestyle changes) should be implemented.
118
4. What is angina, and what causes it?
Angina is severe chest pain caused by inadequate blood supply to the heart, commonly due to atheromatous plaque buildup leading to coronary artery narrowing. Other causes include anemia, aortic stenosis, tachyarrhythmias, hypertrophic cardiomyopathy, and small vessel disease.
119
What distinguishes stable angina from other types of angina?
Stable angina occurs when there is over 70% stenosis of a coronary artery, leading to symptoms during physical or emotional stress, whereas it remains asymptomatic at rest.
120
What is Prinzmetal (vasospastic) angina, and how does it differ from stable angina?
Prinzmetal angina is caused by vasospasm of coronary vessels, typically affecting young women at rest rather than during exertion. It is associated with ST-segment elevation on ECG due to transmural ischemia, unlike stable angina.
121
What is the classic triad of symptoms for stable angina?
The classic triad includes substernal pain or pressure exacerbated by stress/exertion, relieved by rest or nitrates, with pain lasting usually 1-5 minutes.
122
What are the key clinical features associated with stable angina?
Key features include gradual onset of pain, potential radiation to the neck or arm, and associated symptoms like shortness of breath, nausea, dizziness, and lightheadedness.
123
What lifestyle changes can help manage stable angina?
Management includes reducing risk factors associated with ischemic heart disease (IHD), such as smoking cessation, healthy diet, and regular exercise.
124
What is the first-line diagnostic test for stable angina?
An ECG is the first-line test for chest pain; however, it is usually normal in stable angina but may show signs of past myocardial infarction (MI) or ST-segment depression.
125
What are the steps in diagnosing stable angina?
Diagnosis includes:
ECG: Normal in stable angina.
Cardiac enzyme tests: Should be normal.
Stress testing: Exercise or pharmacologic stress test.
Coronary angiography: Definitive test for coronary artery disease (CAD).
126
How is Prinzmetal angina diagnosed?
Coronary angiography is definitive and can show vasospasm when provoked with IV ergonovine or acetylcholine.
127
What are the main treatment strategies for stable and vasospastic angina?
Treatment strategies aim to reduce heart oxygen demand (using nitrates, CCBs, beta-blockers) and increase oxygen delivery (using nitrates and CCBs to relieve vasospasm).
128
What specific treatments are recommended for stable angina?
Risk factor management: Lifestyle changes and medication adherence.
Aspirin and β-blockers: Shown to decrease mortality.
Nitroglycerin: Causes vasodilation, reduces preload and cardiac work, thereby reducing oxygen demand.
129
What is the role of nitroglycerin in treating stable angina?
Nitroglycerin acts as a vasodilator, reducing preload and cardiac work, leading to decreased oxygen demand in the heart.
130
What is pulmonary hypertension (PH) and its definition?
Pulmonary hypertension (PH) is defined as elevated pressure in the pulmonary arteries, measured at ≥ 25 mm Hg at rest. It can be idiopathic or secondary to chronic pulmonary or cardiac diseases.
131
What are the potential consequences of untreated pulmonary hypertension?
Over time, PH can lead to structural changes (dilation or hypertrophy) and impaired function of the right ventricle, potentially resulting in cor pulmonale.
132
What is cor pulmonale?
Cor pulmonale is the alteration in structure and function of the right ventricle caused by a primary disorder of the respiratory system, most commonly due to pulmonary hypertension.
133
What are the common symptoms of pulmonary hypertension?
Early stages may be asymptomatic, but later symptoms include dyspnea on exertion, fatigue, cyanosis, and syncope. In advanced cases, the risk of arrhythmias and death increases.
134
What initial diagnostic test is used for pulmonary hypertension?
Echocardiograms are used as the initial non-invasive test to estimate pulmonary artery pressure and assess the right ventricle's structure.
135
What is the most accurate test for diagnosing pulmonary hypertension?
Right heart catheterization provides the definitive diagnosis and measures the mean pulmonary arterial pressure (mPAP).
136
What are some clinical features of pulmonary hypertension?
Common clinical features include fatigue, chest pain, dyspnea and/or syncope on exertion, a loud and palpable second heart sound, and signs of right-sided heart failure.
137
What classifications of pulmonary hypertension exist according to the WHO?
Group 1: Pulmonary arterial hypertension (idiopathic, hereditary) - poor prognosis.
Group 2: Increased pulmonary venous pressure from left-sided heart failure.
Group 3: Hypoxic vasoconstriction from chronic lung disease (e.g., COPD).
Group 4: Chronic thromboembolic disease.
Group 5: Multifactorial etiology.
138
What diagnostic tests can be used for pulmonary hypertension?
Echocardiography: Initial test to estimate pulmonary artery pressure and check for RV hypertrophy/dilation.
Right heart catheterization: Most accurate test.
ECG: May show RV hypertrophy.
Chest X-ray: Can reveal enlarged pulmonary arteries and right heart hypertrophy.
Additional tests: Pulmonary function tests, arterial blood gases, CT imaging, cardiac MRI.
139
What is the first line of treatment for pulmonary hypertension?
Initial treatment focuses on managing underlying causes. This may include supplemental oxygen, diuretics, anticoagulation, digoxin, and exercise recommendations.
140
What pharmacological treatments are used specifically for Group 1 pulmonary hypertension?
Bosentan: Endothelin-A receptor antagonist (oral).
Sildenafil, tadalafil: Phosphodiesterase type 5 inhibitors that increase cGMP, promoting pulmonary artery relaxation.
Prostacyclin analogues: Such as Epoprostenol, administered IV.
141
What is the treatment approach for Group 4 pulmonary hypertension (thromboembolic disease)?
Surgical thrombectomy is the primary treatment. For patients who cannot undergo surgery, anticoagulation and thrombolytics may be alternatives.
142
5. What is Acute Coronary Syndrome (ACS)?
ACS is a spectrum of clinical syndromes caused by plaque disruption or vasospasm, leading to acute myocardial ischemia. It is subdivided into Non-ST-elevated ACS (NSTE-ACS) and ST-elevated ACS (STE-ACS).
143
What are the subdivisions of ACS?
ACS is subdivided into:
Non-ST-elevated ACS (NSTE-ACS), which includes unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI).
ST-elevated ACS (STE-ACS), which includes ST-elevation myocardial infarction (STEMI).
144
How are NSTEMI and unstable angina (UA) differentiated?
NSTEMI and UA are differentiated by the presence of cardiac biomarkers. NSTEMI shows elevated biomarkers like troponin and CK-MB, indicating myocardial necrosis, while UA shows no elevation in biomarkers.
145
What is the clinical significance of unstable angina (UA)?
Unstable angina is a form of myocardial ischemia that appears at rest or with light exercise without cardiomyocyte necrosis. It signals impending myocardial infarction (MI) due to plaque instability but has no elevated biomarkers.
146
What is NSTEMI, and how does it present?
NSTEMI stands for Non-ST-elevation myocardial infarction, which indicates myocardial necrosis (elevated troponin and CK-MB) without ST-segment elevation on ECG. It typically presents with chest pain that is new, worsening, or occurs at rest.
147
What is STEMI, and how does it occur?
STEMI (ST-elevation myocardial infarction) occurs due to the rupture of an atherosclerotic plaque that forms an occlusive thrombus, leading to prolonged myocardial ischemia and necrosis. It is marked by ST-segment elevations and tall-peaked T waves.
148
What are the key clinical features of ACS?
Acute retrosternal chest pain: dull, squeezing, pressure, or tightness radiating to chest, shoulder, neck, jaw, or arm.
Other symptoms: dyspnea, nausea, vomiting, syncope, sweating.
Atypical symptoms: sharp or no pain (silent MI) in elderly, diabetics, and women.
149
What is the best predictor of survival in STEMI patients?
The best predictor of survival in STEMI patients is left ventricular ejection fraction (LVEF).
150
What is the difference between NSTEMI and STEMI in terms of infarction?
NSTEMI is a subendocardial infarct (partial obstruction of a coronary artery), while STEMI is a transmural infarct (complete or significant obstruction of a coronary artery).
151
What are the autonomic symptoms associated with ACS?
Autonomic symptoms associated with ACS include sweating, nausea, vomiting, and lightheadedness.
152
In which populations might ACS present atypically, and how?
ACS may present atypically in elderly patients, diabetics, and women. Symptoms can include sharp or stabbing chest pain or no pain at all ("silent MI").
153
154
What is Acute Coronary Syndrome (ACS)?
ACS is a spectrum of clinical syndromes caused by plaque disruption or vasospasm, leading to acute myocardial ischemia. It is subdivided into Non-ST-elevated ACS (NSTE-ACS) and ST-elevated ACS (STE-ACS).
155
What are the subdivisions of ACS?
ACS is subdivided into:
Non-ST-elevated ACS (NSTE-ACS), which includes unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI).
ST-elevated ACS (STE-ACS), which includes ST-elevation myocardial infarction (STEMI).
156
How are NSTEMI and unstable angina (UA) differentiated?
NSTEMI and UA are differentiated by the presence of cardiac biomarkers. NSTEMI shows elevated biomarkers like troponin and CK-MB, indicating myocardial necrosis, while UA shows no elevation in biomarkers.
157
What is the clinical significance of unstable angina (UA)?
Unstable angina is a form of myocardial ischemia that appears at rest or with light exercise without cardiomyocyte necrosis. It signals impending myocardial infarction (MI) due to plaque instability but has no elevated biomarkers.
158
What is NSTEMI, and how does it present?
NSTEMI stands for Non-ST-elevation myocardial infarction, which indicates myocardial necrosis (elevated troponin and CK-MB) without ST-segment elevation on ECG. It typically presents with chest pain that is new, worsening, or occurs at rest.
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What is STEMI, and how does it occur?
STEMI (ST-elevation myocardial infarction) occurs due to the rupture of an atherosclerotic plaque that forms an occlusive thrombus, leading to prolonged myocardial ischemia and necrosis. It is marked by ST-segment elevations and tall-peaked T waves.
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What are the key clinical features of ACS?
Acute retrosternal chest pain: dull, squeezing, pressure, or tightness radiating to chest, shoulder, neck, jaw, or arm.
Other symptoms: dyspnea, nausea, vomiting, syncope, sweating.
Atypical symptoms: sharp or no pain (silent MI) in elderly, diabetics, and women.
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What is the best predictor of survival in STEMI patients?
The best predictor of survival in STEMI patients is left ventricular ejection fraction (LVEF).
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What is the difference between NSTEMI and STEMI in terms of infarction?
NSTEMI is a subendocardial infarct (partial obstruction of a coronary artery), while STEMI is a transmural infarct (complete or significant obstruction of a coronary artery).
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What are the autonomic symptoms associated with ACS?
Autonomic symptoms associated with ACS include sweating, nausea, vomiting, and lightheadedness.
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In which populations might ACS present atypically, and how?
ACS may present atypically in elderly patients, diabetics, and women. Symptoms can include sharp or stabbing chest pain or no pain at all ("silent MI").
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What is the diagnostic algorithm for Acute Coronary Syndrome (ACS)?
The diagnostic algorithm for ACS involves a combination of clinical presentation, ECG findings, and myocardial necrosis markers. For NSTE-ACS, it includes unstable angina (no biomarkers) and NSTEMI (elevated biomarkers). For STE-ACS, it is diagnosed with ST-elevation on ECG and elevated troponin levels.
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How is Unstable Angina diagnosed in NSTE-ACS?
Unstable Angina is diagnosed by:
No elevated biomarkers.
ECG showing ST-depression and negative T waves.
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How is NSTEMI diagnosed?
NSTEMI is diagnosed by:
Elevated biomarkers (Troponin I, T, CK-MB) using high-sensitivity cardiac troponin assays.
ECG showing ST-depression and T-wave inversion.
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What is the role of the GRACE score in diagnosing NSTE-ACS?
The GRACE score is used to assess the mortality risk in NSTE-ACS based on factors like age, heart rate, systolic pressure, creatinine, Killip class, biomarker levels, ST deviations, and potential cardiac arrest. It helps confirm or exclude NSTEMI diagnosis.
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What ECG changes indicate an acute STEMI (STE-ACS)?
ECG changes in STEMI include:
Early: ST-elevation, tall T-waves, or new LBBB.
Later: T-wave inversion, pathologic Q-waves. The sequence of changes is tall T-waves → ST-elevation → Q-waves → inverted T-waves → ST normalization → T normalization.
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What are the specific ECG leads indicating different types of myocardial infarctions?
Inferior MI (RCA/PDA): ST-elevation in leads II, III, and aVF.
Anterior MI (LAD): ST-elevation in leads V1–V4.
Lateral MI (LCA): ST-elevation in leads I, aVL, V5–V6.
Posterior MI: ST-depression in leads V1–V2, confirmed with posterior leads V7–V9.
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Which cardiac enzyme is most sensitive and specific for ACS diagnosis?
Troponin is the most sensitive and specific cardiac enzyme for diagnosing ACS. It remains elevated longer than CK-MB, making it more reliable for long-term detection.
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Why is CK-MB useful in the detection of secondary MIs?
CK-MB is useful for detecting secondary MIs because it has a shorter half-life than troponin and returns to normal levels quicker, allowing it to detect new infarcts in patients with recurrent chest pain.
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What is the treatment algorithm for ACS?
Treat symptoms (chest pain, breathlessness).
Pharmacological inhibition of platelet aggregation and anticoagulation (e.g., heparin).
Coronary revascularization, ideally via percutaneous coronary intervention (PCI).
Continuous monitoring (rhythm, hemodynamics, blood gas parameters).
Treat complications.
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What is the primary treatment for STEMI in the ACS treatment algorithm?
For STEMI, the primary treatment is PCI (percutaneous coronary intervention) if possible. If PCI is delayed (>120 minutes) or not possible, fibrinolysis is used, with rescue or facilitated PCI performed if necessary.
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What is the recommended procedural access for PCI in STEMI and NSTEMI?
The radial artery is the recommended procedural access for PCI in both STEMI and NSTEMI cases. It involves opening and dilating the occluded vessel and implanting a drug-eluting stent.
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What is myocarditis and which population is commonly affected?
Myocarditis is an inflammatory disease of the myocardium, often affecting young patients and accounting for approximately 10% of sudden deaths in young adults. It is commonly caused by viral infections or acute rheumatic fever.
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What are the clinical features of myocarditis?
Many patients are asymptomatic, but symptoms can include:
Fatigue, fever, chest pain.
Signs of pericarditis, congestive heart failure (CHF).
Arrhythmias due to inflammation of pacemaker cells.
Sudden cardiac death in severe cases.
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How is myocarditis diagnosed?
Diagnosis of myocarditis includes:
ECG: Sinus tachycardia, concave ST-segment elevations.
Echocardiography: Ventricular dilation, reduced ejection fraction (EF), wall motion abnormalities.
Chest X-ray: Cardiac enlargement, pulmonary congestion, pleural effusion.
Blood cultures and lab tests: Elevated cardiac enzymes, ESR, CRP, BNP, and viral serology.
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What are the treatment options for myocarditis?
Treatment depends on the cause:
Bacterial or fungal: Antibacterial or antifungal therapy.
Viral: Bed rest.
Arrhythmias and heart failure: Appropriate drug therapy (e.g., amiodarone for arrhythmias, β-blockers for heart failure).
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What is the prognosis for myocarditis?
Adults: Most adults with viral myocarditis make a full recovery.
Infants and small children: Prognosis is worse, with only a 25% survival rate.
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What is rheumatic fever and what causes it?
Rheumatic fever is an inflammatory disease affecting the heart, joints, skin, and central nervous system. It occurs 2–4 weeks after an untreated infection with group A streptococcus (GAS). The immune response involves molecular mimicry between streptococcal M proteins and human cardiac proteins, leading to tissue injury and inflammation.
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What are the key clinical features of rheumatic fever?
Clinical features include:
Fever, malaise, and fatigue.
JONES criteria:
Joints: Migratory polyarthritis.
O (Heart): Pancarditis (inflammation of all heart layers) with valvular lesions.
Nodules: Subcutaneous collagen nodules.
Erythema marginatum: Rash with red margins.
Sydenham chorea: Rapid, involuntary movements.
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What is the pathomechanism behind rheumatic fever?
After infection with group A β-hemolytic streptococcus, the bacterial M protein triggers the immune system to produce antibodies. These antibodies mistakenly target proteins in the myocardium and heart valves due to molecular mimicry, causing inflammation and tissue damage (type 2 hypersensitivity reaction).
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How is rheumatic fever diagnosed?
Diagnosis is based on the JONES criteria and lab tests:
Elevated inflammatory markers (ESR, CRP).
Positive antistreptococcal antibody tests (e.g., anti-streptolysin O and antistreptococcal DNAse B titer).
Echocardiogram may reveal mitral or aortic regurgitation.
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What are the treatment options for rheumatic fever?
Treatment includes:
Bed rest to reduce strain on the heart.
Antibiotics (e.g., oral penicillin V) to eradicate the streptococcal infection.
Salicylates (Aspirin) to reduce fever and relieve joint pain.
Corticosteroids for severe joint inflammation (if needed).
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What is the long-term complication of rheumatic fever?
Acute rheumatic fever can lead to chronic rheumatic heart disease, characterized by progressive and permanent damage to the heart valves (especially the mitral valve), potentially causing valvular heart disease.
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What is the goal of prophylaxis in rheumatic fever?
The goal of prophylaxis is to prevent cardiac complications.
Primary prophylaxis: Antibiotic treatment for group A streptococcal infections to prevent rheumatic fever.
Secondary prophylaxis: Antibiotic administration after an episode of acute rheumatic fever to prevent recurrence.
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What are Aschoff bodies and Anitschow cells, and in which condition are they found?
Aschoff bodies are fibrinoid nodules, and Anitschow cells are large macrophages found in the myocardium during rheumatic fever, particularly in cases of myocarditis.
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6. What are the prehospital drug therapy options for acute coronary syndrome?
Administer oxygen if O2 saturation is less than 90%.
Analgesia: IV morphine or metoclopramide.
Low-molecular-weight heparin: To prevent clot formation.
Dual antiplatelet therapy: Aspirin and a P2Y12 inhibitor (usually clopidogrel).
Nitrates: IV or sublingual to relieve chest pain.
β-blockers: Consider if hypertensive or tachycardic (only if no heart failure or cardiogenic shock).
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What are the hospital therapy options for STEMI in acute coronary syndrome?
Emergency angiography and PCI: Should be performed within 90 minutes (door-to-balloon time).
If PCI cannot be performed in time, fibrinolysis is recommended.
Post-PCI: Administer dual antiplatelet therapy (aspirin and clopidogrel).
Long-term treatment: Aspirin, ACE inhibitors, β-blockers, nitrates, and high-dose statins.
Address modifiable risk factors.
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What is the treatment approach for NSTEMI/UA in acute coronary syndrome?
Invasive strategy (for high- to intermediate-risk patients): Coronary angiography within 2–72 hours.
Ischemia-guided strategy (for stable, low-risk patients): Further testing (exercise ECG, stress echocardiography) to evaluate the need for coronary angiography.
Management depends on mortality risk (e.g., TIMI score) and clinical findings.
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What is the role of β-blockers in prehospital treatment of acute coronary syndrome?
β-blockers should be considered if the patient is hypertensive or tachycardic and not in heart failure or cardiogenic shock. If the patient is in heart failure or shock, ACE inhibitors are recommended (unless the patient is hypotensive).
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When is urgent cardiac surgery indicated in acute coronary syndrome?
Urgent cardiac surgery is performed in case of mechanical complications, such as:
Interventricular septum rupture.
Papillary muscle rupture.
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What are the criteria for performing PCI in STEMI during acute coronary syndrome?
PCI should be performed within 90 minutes (door-to-balloon time) if possible. If PCI is delayed beyond 90 minutes, fibrinolysis is recommended.
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What medications are used long-term after a PCI in acute coronary syndrome?
After PCI, long-term medications include:
Aspirin.
ACE inhibitors.
β-blockers.
Nitrates.
High-dose statins.
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What is infective endocarditis (IE)?
Infective endocarditis (IE) is an infectious inflammation of the endocardium, primarily affecting the heart valves. It is caused by bacteremia from sources like dental procedures, surgery, or nonsterile injections.
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What are the two types of infective endocarditis based on disease progression?
Acute IE: Caused by Staphylococcus aureus, rapid onset, and destructive.
Subacute IE: Caused by viridans streptococci, slow progression, affects pre-damaged or prosthetic valves.
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What are common causes of acute and subacute infective endocarditis?
Acute IE: Caused by Staphylococcus aureus; affects previously healthy valves.
Subacute IE: Caused by viridans streptococci; usually affects previously damaged valves, often following dental procedures.
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What are the typical clinical features of infective endocarditis?
Constitutional symptoms: Fever, chills, malaise, night sweats, weight loss.
Cardiac signs: New or changed murmur, arrhythmias, signs of heart failure.
Peripheral signs (FROM JANE):
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Nail-bed hemorrhages
Emboli
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What does the acronym FROM JANE stand for in infective endocarditis?
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhages
Emboli
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What is the diagnostic criteria for infective endocarditis?
Diagnosis is made using the Duke criteria, which includes:
Positive blood cultures.
Evidence of endocardial involvement via echocardiography (TTE, then confirm with TEE).
Lab tests: Elevated ESR, CRP
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What pathogens most commonly cause infective endocarditis?
Staphylococcus aureus: Causes acute IE, affects healthy valves.
Viridans streptococci: Causes subacute IE, commonly affects damaged valves, especially after dental procedures.
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What are the treatment options for infective endocarditis caused by different pathogens?
Penicillin-susceptible streptococci: Penicillin.
Penicillin-resistant streptococci: Amoxicillin/ceftriaxone + aminoglycoside, clindamycin.
Staphylococcus aureus: Methicillin, oxacillin.
MRSA: Vancomycin.
Gram-negative HACEK bacteria: Ceftriaxone, quinolones.
Fungi: Amphotericin B, fluconazole.
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What are key complications of untreated infective endocarditis?
Untreated infective endocarditis can be fatal within weeks due to complications like heart failure, embolic events (stroke, septic emboli), and valve destruction.
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What is the role of echocardiography in diagnosing infective endocarditis?
Echocardiography helps detect valve vegetations, regurgitation, and abscesses.
Start with TTE (transthoracic echocardiogram), and confirm with TEE (transesophageal echocardiogram) if needed.
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7. What is the goal of primary prevention of myocardial infarction (MI)?
Primary prevention aims to treat asymptomatic high-risk patients by identifying and managing modifiable risk factors to prevent future cardiovascular events.
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What are the components of risk assessment in primary prevention of MI?
Risk assessment involves identifying individuals at high or very high cardiovascular risk and providing preventive care, using tools like the SCORE chart to assess 10-year cardiovascular mortality risk based on factors like gender, age, smoking status, blood pressure, and cholesterol levels.
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What lifestyle changes are recommended for primary prevention of MI?
Recommended lifestyle changes include a Mediterranean diet low in trans fats, complete smoking cessation, regular aerobic exercise, and weight loss.
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What major risk factors should be controlled for primary prevention of MI?
Control of major risk factors includes managing blood pressure, blood sugar (strict HbA1c control), and cholesterol levels through lipid-lowering drugs (statins, ezetimibe, PCSK9 inhibitors) and a low-fat diet.
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In what cases is low-dose aspirin recommended for primary prevention of MI?
Low-dose aspirin may be beneficial in high-risk groups to help prevent blood clot formation and reduce cardiovascular events.
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What is the goal of secondary prevention of MI?
Secondary prevention aims to prevent recurrence of MI by slowing the progression of atherosclerosis, stabilizing existing plaques, and promoting plaque regression in patients with established cardiovascular disease.
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What pharmacological therapies are recommended for secondary prevention of MI?
Recommended therapies include lifelong low-dose aspirin or dual antiplatelet therapy (e.g., aspirin/clopidogrel), β-blockers, statins, ACE inhibitors (ACEIs) or ARBs, and aldosterone antagonists for specific heart failure or diabetic patients.
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What are the benefits of involving patients in cardiac rehabilitation programs?
Cardiac rehabilitation programs help educate patients, encourage lifestyle changes, ensure medication adherence, and promote long-term cardiovascular health.
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Why is it important to control modifiable risk factors in the prevention of MI?
Controlling modifiable risk factors like hypertension, diabetes, and hyperlipidemia reduces the risk of atherosclerosis progression, helps prevent cardiovascular events, and improves overall heart health.
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How do β-blockers contribute to secondary prevention of MI?
β-blockers reduce heart workload, lower blood pressure, prevent arrhythmias, and help improve survival in post-MI patients unless contraindicated.
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What role does patient education play in MI prevention?
Patient education is crucial for engaging individuals in their care, ensuring adherence to lifestyle modifications, and improving outcomes in both primary and secondary prevention of MI.
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What is the role of statins in preventing MI?
Statins lower cholesterol levels, stabilize atherosclerotic plaques, and reduce the risk of cardiovascular events, making them essential in both primary and secondary prevention of MI.
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What is mitral regurgitation (MR)?
Mitral regurgitation (MR) is the leakage of blood from the left ventricle (LV) into the left atrium (LA) due to incomplete closure of the mitral valve during systole.
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What are the two main types of mitral regurgitation?
The two main types are primary (organic) MR, caused by direct involvement of the mitral valve, and secondary (functional) MR, caused by changes in the left ventricle that lead to valvular incompetence.
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What are common causes of primary (organic) mitral regurgitation?
Causes include degenerative mitral valve disease (mitral valve prolapse, calcification, chordae tendineae rupture), rheumatic fever, infective endocarditis, and ischemic MR (papillary muscle rupture post-MI).
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What is secondary (functional) mitral regurgitation?
Secondary MR is caused by changes in the left ventricle, such as coronary artery disease, dilated cardiomyopathy, or left-sided heart failure, which stretch the mitral valve annulus, leading to valvular incompetence.
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What are the common symptoms of mitral regurgitation?
Symptoms include dyspnea, orthopnea, fatigue, and possibly signs of pulmonary edema or left-sided heart failure.
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What is the characteristic sound of mitral regurgitation on auscultation?
A holosystolic, high-pitched blowing murmur radiating to the axilla, potentially accompanied by an S3 heart sound.
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What is the preferred diagnostic method for mitral regurgitation?
Transthoracic echocardiography is the preferred method, used to assess LV function, LA dimensions, pulmonary pressures, and the severity of regurgitation.
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What additional imaging method can help assess the severity of mitral regurgitation?
Angiography can be used to help assess the severity of mitral regurgitation.
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What is the definitive treatment for primary mitral regurgitation?
Surgical repair or valve replacement is the definitive treatment for primary mitral regurgitation.
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How is secondary mitral regurgitation treated?
Treatment of secondary MR focuses on addressing the underlying condition (e.g., treating heart failure or cardiomyopathy), along with pharmacological therapy to reduce heart failure severity.
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What medications may help improve symptoms and reduce the progression of mitral regurgitation?
Diuretics, beta-blockers (βB), and ACE inhibitors (ACEI) may help improve symptoms and reduce the rate of progression of mitral regurgitation.
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When is anticoagulation therapy indicated in mitral regurgitation patients?
Anticoagulation therapy is indicated in patients with mitral regurgitation who have atrial fibrillation (AF).
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When is mitral valve surgery indicated in symptomatic patients with mitral regurgitation?
Mitral valve surgery is indicated in symptomatic patients with significant primary mitral regurgitation (grade III-IV).
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What are the criteria for intervention in asymptomatic patients with significant mitral regurgitation?
Intervention is indicated if systolic pulmonary pressure is ≥50 mmHg, left ventricular ejection fraction (LVEF) is ≤60%, left ventricular end-systolic diameter (LVESD) is ≥45 mm, or there is new-onset atrial fibrillation (AF).
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What are the two main surgical treatment options for mitral regurgitation?
The two main treatment options are mitral valve repair or mitral valve replacement.
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What is a special consideration in the treatment of secondary mitral regurgitation?
In secondary mitral regurgitation, a surgical approach (valvuloplasty) is controversial and is usually performed with concomitant revascularization. Percutaneous edge-to-edge repair (mitral clip) can improve symptoms and quality of life.
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What are common complications of mitral regurgitation?
Complications include heart failure, pulmonary edema, atrial fibrillation, and arterial emboli.
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8. What are the most common early complications of myocardial infarction within the first 24 hours?
Early complications include arrhythmias (ventricular fibrillation, ventricular tachycardia, AV block, asystole, atrial fibrillation), sudden cardiac death, acute left heart failure, and cardiogenic shock.
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What are the two most common types of arrhythmias following an acute myocardial infarction?
Ventricular fibrillation (VF) and ventricular tachycardia (VT) are the most common arrhythmias and leading causes of sudden cardiac death (SCD) after an acute myocardial infarction.
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When does pericarditis typically occur as a complication of myocardial infarction?
Pericarditis typically occurs 1-3 days after a large myocardial infarction due to inflammation caused by neutrophil infiltration.
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What are common complications that can occur between 3-14 days after a myocardial infarction?
Complications between 3-14 days include papillary muscle rupture, ventricular septal rupture, left ventricular free wall rupture, and left ventricular pseudoaneurysm.
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What complication of myocardial infarction leads to mitral regurgitation and when does it typically occur?
Papillary muscle rupture, typically occurring 2-7 days after myocardial infarction, can lead to mitral regurgitation.
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What complication, most commonly caused by left anterior descending (LAD) artery infarction, occurs 3-5 days post-myocardial infarction?
Ventricular septal rupture, most commonly caused by LAD artery infarction, occurs 3-5 days post-MI.
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What late complications of myocardial infarction occur 2 weeks to months after the event?
Late complications include atrial and ventricular aneurysms, Dressler syndrome, congestive heart failure, and reinfarction.
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What is Dressler syndrome and when does it occur following a myocardial infarction?
Dressler syndrome is an autoimmune pericarditis occurring 2-10 weeks post-MI. It presents with pleuritic chest pain, fever, and diffuse ST elevation. Treatment includes NSAIDs and colchicine.
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How is a ventricular aneurysm detected and what complications can arise from it?
A ventricular aneurysm is detected by echocardiography, showing dyskinetic movements of the thinned wall. Complications include rupture, cardiac tamponade, and mural thrombus formation.
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What is the mnemonic "DARTH VADER" used for in the context of myocardial infarction complications?
"DARTH VADER" stands for:
Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valvular disease
Aneurysm of ventricle
Dressler’s syndrome
Emboli
Recurrence/reinfarction/regurgitation (mitral)
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What is mitral stenosis and what is its most common cause?
Mitral stenosis (MS) is a valvular anomaly that obstructs blood flow from the left atrium (LA) to the left ventricle (LV). The most common cause is rheumatic fever.
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What happens in the early stages of mitral stenosis?
In early stages of mitral stenosis, reduced mitral valve opening leads to dilation of the left atrium and progressive congestion of the lungs, which can eventually cause cardiac asthma and pulmonary edema.
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What are the main causes of mitral stenosis?
The main causes of mitral stenosis are:
Rheumatic fever (most common, due to commissural fusion)
Degenerative calcification
Autoimmune diseases (e.g., systemic lupus erythematosus, rheumatoid arthritis)
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What are the common symptoms of mitral stenosis?
Common symptoms of mitral stenosis include:
Dyspnea (due to pulmonary congestion)
Orthopnea
Hemoptysis
Chest pain
Palpitations
Thromboembolic complications (due to atrial fibrillation)
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What heart sounds are characteristic of mitral stenosis?
In mitral stenosis, the characteristic heart sounds include a loud S1, an opening snap after S2, and a mid-diastolic murmur.
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What is the preferred method of diagnosis for mitral stenosis and what parameters are measured?
The preferred diagnostic method for mitral stenosis is echocardiography. It measures mitral valve area, transvalvular diastolic gradient, and pulmonary pressures. A mitral valve area <1.5 cm² indicates severe mitral stenosis.
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What findings might a chest X-ray reveal in a patient with mitral stenosis?
A chest X-ray may reveal left atrial enlargement in a patient with mitral stenosis.
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What are the medical treatment options for mitral stenosis?
Medical treatment options for mitral stenosis include diuretics, beta-blockers (βB), digoxin, or heart rate-regulating calcium channel blockers (CCB) to improve symptoms. Anticoagulation is indicated for patients with atrial fibrillation.
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When is mitral valve surgery or commissurotomy indicated in mitral stenosis?
Mitral valve surgery or commissurotomy is indicated in symptomatic patients with clinically significant mitral stenosis, especially if the valve area is less than 1.5 cm².
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What are the treatment options for non-severe and severe mitral stenosis?
For non-severe mitral stenosis, percutaneous balloon commissurotomy is the first-line treatment. In more severe cases, surgical valve replacement is needed.
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9. What is the importance of differentiating the causes of nontraumatic chest pain in an emergency setting?
Differentiating the causes of nontraumatic chest pain is crucial because some conditions, such as acute coronary syndrome and pulmonary embolism, are life-threatening and require immediate evaluation and treatment.
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What are the key categories in the differential diagnosis of chest pain?
The differential diagnosis of chest pain includes cardiac, gastrointestinal (GI), musculoskeletal, and psychiatric etiologies.
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What key questions should be asked when evaluating a patient with chest pain?
Key questions include:
Frequency of pain
Duration of pain
Location of pain
Quality of pain (what kind of pain)
Radiation of pain
Severity of pain (on a scale of 1 to 10)
What makes the pain better or worse
Associated symptoms
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What should guide the diagnostic workup for chest pain after life-threatening causes have been ruled out?
After life-threatening causes have been ruled out, the diagnostic workup for chest pain should be guided by a thorough history, physical examination, and the pretest probability of the diagnoses under consideration.
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What initial diagnostic tools are essential in evaluating chest pain?
Initial diagnostic tools include laboratory tests, physical examination, and a 12-lead ECG to help assess the cause of chest pain.
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What is the purpose of pacemakers?
Pacemakers are implanted to help control the heartbeat, either temporarily after events like a heart attack, surgery, or medication overdose, or permanently to correct a slow or irregular heartbeat or help treat heart failure.
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What are the three types of pacemakers?
The three types of pacemakers are:
Permanent implantable system for long-term treatment
Temporary transcutaneous (with electrode pads over the chest)
Temporary transvenous
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What is a key feature of cardiac pacing noted on an ECG?
A key feature of cardiac pacing noted on an ECG is the presence of a "spike," indicating electrical stimulation of the heart by the pacemaker.
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What are the main indications for pacemaker treatment?
The main indications for pacemaker treatment include:
Sinus node dysfunction (most common)
Second-degree block type II
Complete heart block (third-degree block)
Symptomatic bradyarrhythmias
Tachyarrhythmias (to interrupt rapid rhythm disturbances)
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How are pacemakers classified?
Pacemakers are classified according to the chamber being paced (stimulated), chamber sensed, response to sensing, and rate response.
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What are the two approaches for implanting pacemakers?
The two approaches for implanting pacemakers are the endocardial (transvenous) approach and the epicardial approach.
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Which approach for pacemaker implantation is most common and what does it involve?
The endocardial (transvenous) approach is the most common method. It involves administering a local anesthetic, making an incision in the chest, inserting leads through the incision into a vein, and guiding them to the heart using fluoroscopy.
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In which patients is the epicardial approach for pacemaker implantation more common?
The epicardial approach is more common in children, and it involves the use of general anesthesia.
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What is an implantable cardioverter defibrillator (ICD) and its purpose?
An ICD is an implanted device that continuously monitors the heart and prevents sudden cardiac death by delivering electrical impulses to convert the heart rhythm back into sinus rhythm.
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What are the indications for using an ICD?
ICDs are indicated in patients with ischemic heart disease and EF <30%, heart failure (HF) class II-IV patients with EF <35%, and in patients with life-threatening arrhythmias.
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How does defibrillation work and what conditions does it treat?
Defibrillation delivers a shock that is not in synchrony with the QRS complex and is effective for treating ventricular fibrillation (VFib) and ventricular tachycardia (VT) without a pulse.
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What is cardiac resynchronization therapy (CRT) and when is it used?
Cardiac resynchronization therapy (CRT) involves a three-chamber cardiac pacemaker used in symptomatic chronic heart failure (HF) to synchronize all the chambers. It is indicated in HF class II-IV patients with EF <35%, dilated cardiomyopathy, and left bundle branch block (LBBB) with QRS >150 ms.
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Can cardiac resynchronization therapy (CRT) be combined with other devices?
Yes, cardiac resynchronization therapy (CRT) may be combined with an implantable cardioverter defibrillator (ICD).
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10. What is the first step in the treatment of congestive heart failure (CHF)?
The first step in the treatment of CHF is lifestyle modifications and patient education.
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What are some lifestyle modifications recommended for patients with CHF?
Lifestyle modifications include salt restriction (<3g/day), fluid restriction (<2L), weight loss and exercise, cessation of smoking and alcohol, and daily weight monitoring to detect fluid retention.
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What is the aim of pharmacotherapy in the treatment of CHF?
Pharmacotherapy aims to decrease preload, decrease afterload, increase contractility, and decrease cardiac remodeling.
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What is the first-line pharmacological treatment for CHF?
First-line treatment includes loop diuretics for volume overload, ACE inhibitors (ACEIs) to reduce preload and afterload, and beta-blockers added once the patient is stable on ACEI.
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What medications can be added as second-line treatment for CHF?
Second-line treatments include ivabradine (if symptomatic after max β-blocker dose), hydralazine (if EF <40% or ACEIs are not tolerated), angiotensin receptor-neprilysin inhibitors, and digoxin.
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What are contraindicated drugs in CHF treatment?
Contraindicated drugs include NSAIDs, calcium channel blockers, and antidepressants.
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What is an implantable cardioverter defibrillator (ICD) and its indications?
An ICD is a device that prevents sudden cardiac death by delivering electrical impulses. It is indicated for patients with ischemic heart disease and EF <30%, HF Class II-IV with EF <35%, and those at increased risk of life-threatening arrhythmias.
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What is cardiac resynchronization therapy (CRT) and when is it used?
CRT is a three-chamber cardiac pacemaker used in symptomatic chronic HF (Class II-IV with EF <35%, dilated cardiomyopathy, and LBBB with QRS >150ms) to improve cardiac function. It can be combined with an ICD.
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What is the role of a Left Ventricular Assist Device (LVAD) in CHF treatment?
An LVAD is a pump that supports ventricular function and may be used temporarily or long-term until transplantation.
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In what cases is a heart transplant indicated?
A heart transplant is indicated for Class IV end-stage CHF patients with EF <20%.
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What is cardiac toxicity, and what can cause it?
Cardiac toxicity refers to damage to the heart caused by harmful chemicals, often as a side effect of cancer treatments such as chemotherapy (e.g., anthracyclines like doxorubicin, cyclophosphamide), targeted therapy (e.g., trastuzumab), and radiation therapy.
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Who is at increased risk for cardiac toxicity?
Patients at increased risk include older adults, young children, women, and those with other health conditions or pre-existing heart issues.
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What are common symptoms of cardiac toxicity?
Most patients are asymptomatic, but symptoms may occur if cardiac toxicity leads to reduced left ventricular ejection fraction (LVEF) or congestive heart failure (CHF).
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How is cardiac toxicity diagnosed?
Diagnosis includes a physical examination, chest X-ray, echocardiogram, and ECG.
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What preventive measures can reduce cardiac toxicity during cancer treatment?
Preventive measures include administering lower doses of cancer drugs more frequently, using less toxic drug formulations (e.g., liposomal doxorubicin), and considering prophylactic use of ACE inhibitors and beta-blockers.
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What are the treatments for cardiac toxicity?
Treatments may include diuretics, ACE inhibitors, beta-blockers, and digitalis.
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How are cardiac tumors classified?
Cardiac tumors can be classified as benign (non-cancerous) or malignant (cancerous), and further categorized as primary (originating within the heart) or secondary (metastasis from another part of the body).
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What is the prevalence of primary cardiac tumors?
Primary cardiac tumors are extremely rare, occurring in approximately 1 in 3000 individuals, with 75% being benign. Secondary tumors are 20-30 times more common.
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What are some clinical presentations of cardiac tumors?
Clinical presentations include heart failure, arrhythmias, chest pain, stroke, pericardial effusion, fatigue, dyspnea, weight loss, and syncope.
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How are cardiac tumors diagnosed?
Diagnosis is commonly done by echocardiogram, with additional imaging studies such as CT, MRI, and catheterization as needed.
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What is the most common primary cardiac tumor?
Myxoma is the most common primary cardiac tumor, often found in the left atrium, and can cause mitral stenosis or regurgitation.
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What are other common primary cardiac tumors?
Other common primary tumors include papillary fibroelastoma (affecting valves), rhabdomyoma (common in children), fibroma (also in children), lipoma, and hemangioma.
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What is the general treatment for primary cardiac tumors?
Surgical resection is generally required for primary cardiac tumors, and if tumors are malignant, chemotherapy should be combined with resection.
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What is the recurrence rate for myxoma after surgical resection?
Myxoma has a reported recurrence rate of 2-5% after surgical resection.
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11. What is heart failure with preserved ejection fraction (HFpEF)?
HFpEF, or diastolic heart failure, occurs when the heart muscle has difficulty relaxing, leading to reduced end-diastolic volume (EDV) and stroke volume (SV) while maintaining a normal ejection fraction (EF > 50%).
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What causes diastolic dysfunction in HFpEF?
Diastolic dysfunction in HFpEF is primarily caused by impaired ventricular relaxation and increased ventricular stiffness. The most common cause is hypertension leading to ventricular hypertrophy.
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Who is the typical patient for HFpEF?
The typical patient with HFpEF is an older woman with a history of hypertension and diabetes mellitus (DM).
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What are the main causes of HFpEF?
Main causes of HFpEF include:
Hypertension (leading to hypertrophy)
Valvular disease (aortic/mitral stenosis or aortic regurgitation)
Restrictive cardiomyopathy
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How is HFpEF diagnosed?
Diagnosis of HFpEF includes:
LVEF > 50%
Elevated BNP (>100 pg/mL) and/or NT-proBNP levels
Echocardiographic evidence of diastolic dysfunction (increased atrial volume index and LV mass)
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What is the significance of elevated BNP in HFpEF?
Elevated BNP levels indicate ventricular strain and fluid overload; however, they may show false negatives in obese patients.
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What are the treatment options for HFpEF?
Treatment options for HFpEF are mainly symptom-based and include:
Diuretics for volume overload
Salt and fluid restrictions, along with daily weight monitoring
ACE inhibitors, ARBs, and beta-blockers to help with symptoms
Optimization of antihypertensive and diabetic treatments
Anticoagulation for patients with atrial fibrillation
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Why is prognosis improvement limited in HFpEF?
Few therapeutic options exist for HFpEF that improve prognosis; most treatments focus on symptom relief rather than addressing the underlying diastolic dysfunction.
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What is atherosclerosis?
Atherosclerosis is the most common type of arteriosclerosis characterized by the thickening and stiffening of the arterial wall due to cholesterol plaque buildup in the intima.
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What are the major risk factors for atherosclerosis?
Major risk factors include:
Smoking
Diabetes mellitus
Arterial hypertension
Dyslipidemia
Family history of early heart disease
Advanced age
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Describe the pathogenesis of atherosclerosis.
Atherosclerosis begins with endothelial damage, leading to inflammation, the invasion of inflammatory cells, and platelet adhesion. Smooth muscle cells and macrophages take up oxidized LDL, becoming foam cells. These foam cells accumulate, forming fatty streaks and triggering extracellular matrix production, leading to fibrous plaques that can rupture and cause thrombosis.
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What are common sites of atherosclerosis?
Common sites include:
Abdominal aorta
Coronary arteries
Popliteal arteries
Carotid arteries
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What conditions can result from atherosclerosis?
Conditions caused by atherosclerosis include:
Arterial aneurysms
Dissection
Coronary heart disease (CHD)
Peripheral artery disease (PAD)
Intestinal ischemia
Subcortical vascular dementia (Binswanger's disease)
Thrombosis (acute coronary syndrome and stroke)
Renovascular hypertension
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What is arteriosclerosis?
Arteriosclerosis is a general term for the thickening and stiffening of arterial walls with variable pathogenesis.
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Describe the different types of arteriosclerosis.
Atherosclerosis: Multifactorial inflammatory disease affecting the intima, characterized by cholesterol plaque buildup; affects elastic and large/medium-sized muscular arteries.
Mönckeberg arteriosclerosis: Dystrophic calcification of the media; no blood flow obstruction; affects medium-sized arteries, showing a pipestem appearance on X-ray.
Arteriolosclerosis: Hardening of small arteries and arterioles, which can be:
Hyaline arteriolosclerosis: Protein deposition due to leakage; seen in chronic hypertension, diabetes, and aging.
Hyperplastic arteriolosclerosis: Subendothelial smooth muscle proliferation in response to very high blood pressure, characterized by "onion-skin" appearance; associated with malignant hypertension.
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What is the histological appearance of hyaline arteriolosclerosis?
Hyaline arteriolosclerosis shows pink amorphous deposits (hyaline) within the arteriolar walls on H&E staining, resulting from protein leakage.
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What is the histological appearance of hyperplastic arteriolosclerosis?
Hyperplastic arteriolosclerosis is characterized by an "onion-skin" appearance of the arteriole due to the proliferation of subendothelial smooth muscle cells, typically associated with malignant hypertension.
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What is the primary cause of atherosclerosis?
The primary cause of atherosclerosis is endothelial injury or dysfunction, often due to chronic stress on the endothelium from hemodynamic disturbances, such as increased turbulent flow at branch points.
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What role does inflammation play in atherosclerosis?
Inflammation of the vessel wall is a critical component of atherosclerosis, leading to lipid accumulation and the recruitment of monocytes to the intima.
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How do lipids contribute to atherosclerosis?
Lipids accumulate in the intima, where they are oxidized by free radicals. Macrophages ingest oxidized LDL, transforming into foam cells that form fatty streaks (early atherosclerotic lesions).
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What is the significance of foam cells in atherosclerosis?
Foam cells, formed by macrophages ingesting oxidized LDL, accumulate in the intima, leading to the development of fatty streaks and contributing to plaque formation.
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What growth factors are involved in atherosclerosis?
Platelets and endothelial cells release growth factors such as PDGF, FGF, and TGF-alpha, which stimulate smooth muscle cell proliferation in the intima and the differentiation of fibroblasts into myofibroblasts.
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Describe the development of fibrous plaques (atheromas).
Lipid-laden macrophages and smooth muscle cells produce extracellular matrix components (like collagen), leading to the formation of fibrous plaques. Inflammatory cells secrete matrix metalloproteinases, weakening the fibrous cap.
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What happens when the fibrous cap of an atheroma ruptures?
Rupture of the fibrous cap exposes thrombogenic material, leading to thrombus formation, which can cause vascular occlusion or further thrombotic complications.
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List the common sites of atherosclerosis in order of frequency.
Circle of Willis
Carotid arteries
Popliteal arteries
Coronary arteries
Abdominal aorta
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What is the purpose of the SCORE risk charts?
The SCORE risk charts assess cardiovascular risk based on gender, age, total cholesterol, systolic blood pressure, and smoking status, calculating a patient’s 10-year cardiovascular disease risk.
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What are the main treatment strategies for atherosclerosis?
Management of risk factors (lifestyle changes, smoking cessation)
Medical treatment for hypertension, diabetes, and hyperlipidemia
Interventional techniques:
Angiography and stenting
Angioplasty
Thrombolytic therapy
Bypass surgery
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What are some target organ manifestations of atherosclerosis?
Eye: Retinopathy, optic neuropathy
Heart: Coronary artery disease
Brain: Hypertensive encephalopathy, transient ischemic attack, stroke
Kidney: Nephrosclerosis
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