Ischaemic heart disease: prevalence, symptoms and principles of treatment Flashcards
what is CVD
a disease of the heart or circulatory system which comprises
CHD, Cerebrovascular disease and peripheral vascular disease
What results from CVD
Marked increase in prevalence of CVD during 20th century in Western countries
UK’s second biggest killer – approx a 1/3 of deaths annually
Mainly heart attack and stroke
Significant economic burden
What is the framingham heart study
Ongoing, longitudinal study in 5209 healthy men and women 30-62 yrs in Framingham, MA
Begin in 1948, in 3rd generation of participants
Medical profession had little understanding of CVD prevention before Framingham
1957 high cholesterol and bp link to CHD
1961 Risk factors introduced
1962 smoking and CHD
1967 OBESITY
1972 DIABETES
what are controllable risk factors for CHD
Cigarette smoking Diabetes Bp Cholesterol Obesity
what are noncontrollable risk factors for CHD
Age
Family history of premature CHD
Previous heart attack
what are the clinical manifestations of CHD
Athersclerosis (fatty streak, lipid deposition, intimal fibrosis)
what is IHD (or myocardial ischaemia)
occurs due to atherosclerotic plaque build-up within one or more arteries, obstructing myocardial blood flow
Imbalance between myocardial oxygen supply and demand
Restriction in normal increase in coronary blood flow which should occur with increasing myocardial oxygen demand
what are the clinical manifestations of IHD
Asymptomatic
Stable angina
Acute coronary syndromes – unstable angina, NSTEMI, STEMI
Long term – HF, arrythmias, sudden death
What is the pathology of stable angina
ischaemia due to fixed atheroma stenosis of one or more coronary arteries
What is the pathology of unstable angina
ischaemia caused by dynamic obstructions of a coronary artery due to plaque rupture with thrombosis
What is the pathology of myocardial infarction
acute occlusion of a coronary artery due to plaque rupture and thrombosis
What is the pathology of heart failure
Myocardial dysfunction due to infarction or ischaemia
What is the pathology of arrhythmia
altered conduction due to ischaemia or infarction
What is the pathology of sudden death
ventricular arrhythmia, asystole or massive infarction
what are the types of stable angina
typical, atypical, non-anginal
what are the symptoms of the types of stable anginas
typical meet all 3 of these characteristics
substernal chest discomfort of characteristic quality and duration
provoked by exertion or emotional stress
relieved by rest or nitrates in mins
atypical 2
non-anginal 1 or none
how is stable angina measured
1st line
short acting nitrates and beta-blockers
2nd line if 1st not enough
then stent/CABG/lifestyle/education/aspirin/statins
what are acute coronary symptoms characterised by
Includes unstable angina and acute MIs (stemi and nstemi)
All patients with acute MI have a rise in cardiac enzyme known as troponin, measured on a blood test
Troponin is released into bloodstream following an injury to heart muscle, diagnostic marker (elevated in acute MI but not unstable angina)
what is the pathology of STEMI
ST elevation on ECG is a marker of complete coronary occlusion
what is the pathology of NSTEMI
incomplete occlusion is associated with ST depression, variable T wave abnormalities or normal ECG
What is the pathological progression to atherothrombosis
Plaque disrupted, thrombus results from
Adherence, activation and aggregation of platelets
Thrombin and fibrin produced via coagulation cascade (thrombin release from platelets)
Vasoactive molecules released from platelets which causes vasoconstriction
what are the classical symptoms of ACS
Discomfort/pain in centre of chest for more than a few mins and recurs
Radiates to other areas eg left arm/jaw/back
Occur at rest or exertion
Not relieved immediately with sublingual GTN
Elderly/diabetic often present with
Breathlessness
Nausea or vomiting
Sweating or clamminess
how can patients with suspected ACS be assessed
First – history, ECG, Physical exam
Then risk stratification and cardiac biomarkers (eg troponin)
how can a history for suspected ACS be taken
Nature and site of pain
Time of pain onset and duration
History of CVD/risk factors
what are therapeutic goals in ACS
Restore coronary artery patency (STEMI)
Limit myocardial necrosis (STEMI)
Control symptoms
Medical management
Anti-platelet therapy (aspirin, clopidogrel/prasugrel/ticagrelor)
Anti-ischaemic therapy (nitrates)
Secondary prevention therapy (statin, ACE inhibitors, beta blockers, stop smoking, lifestyle mod)
what is key for treating STEMIs
Timely diagnosis key to successful management
Most critical time is early phase
Minimise delays to treatment associated with improved clinical outcomes
how can STEMIs be treated rapidly
Importance of rapid treatment
Morphine and or nitrates
Anti-platelet agents
And emergency primary angioplasty (balloons or stents)
Clot busting drug (thrombolysis) if no primary angioplasty
what is unstable angina
Angina at rest >20 mins
New onset <2 months exertional angina
Recent <2 months acceleration or progressions
Normal cardiac biomarkers
what is an NSTEMI
No ST elevation but angina and elevated cardiac biomarkers
Pneumonia, pulmonary embolism, pericarditis, sepsis HF, uncontrolled tachycardia can raise troponin too
What are high risk ACS patients
Elevated troponin Renal impairment Recurrent chest pain Dynamic ST depression or T wave changes Haemodynamic instability Major arrythmias HF Elderly
how can NSTEMI be treated
Analgesia Anti platelet Anti ischaemic Statins Early coronary angiography with view to revascularize (eg bypass)
