T2: IHD and Heart Failure

Question 1

How do we prevent IHD?

Answer 1

Prevention: 
• No smoking
• Lose/manage weight
• Lower blood pressure
• Encourage exercise    
Calculate risk and prescribe appropriate agents such as aspirin and statins

Question 2

What is the pathogenesis of IHD?

Answer 2

Clinical manifestation is due to a progressive narrowing of the Coronary artery lumen. This leads to either stenosis (chronic disease) or acute plaque disease due to a thrombosis (acute ischemia). Patients usually experience symptoms induced by exercise once a fixed obstructive lesion reaches 75% or greater, whereas a 90% obstruction can cause ischemia, even at rest.

Question 3

What are disease syndromes of IHD?

Answer 3

• Angina pectoris - Complex of symptoms characterised by paroxysmal attacks of chest pain caused by transient myocardial ischaemia that falls short of inducing the cellular necrosis that defines ischaemia - typically considered to be 3 patterns: typical/stable, crescendo/unstable and variant/prinzmetal angina.
• Acute coronary syndrome
• Sudden cardiac death
• Chronic ischaemic heart disease

Question 4

What is prinzmetal angina?

Answer 4

Occurs at rest and is due to coronary artery spasm (usually ST elevation seen on ECG). Unrelated to exertion, heart rate or blood pressure [simillar to that seen in cocaine use].

Question 5

What is stable angina?

Answer 5

Typical/stable -
symptoms brought on at a predictable level of exertion, relieved by rest / or nitrates (vasodilator).Due to reduction of coronary perfusion to a critical level by chronic narrowing by atherosclerosis

Question 6

What are disease syndromes of IHD?

Answer 6

• Angina pectoris - Complex of symptoms characterised by paroxysmal attacks of chest pain caused by transient myocardial ischaemia that falls short of inducing the cellular necrosis that defines ischaemia - typically considered to be 3 patterns: typical/stable, crescendo/unstable and variant/prinzmental angina.
• Acute coronary syndrome - Non-ST elevation myocardial infarction(NSTEMI),unstable angina, andST-elevation myocardial infarction(STEMI) are the three types of ACS.
• Sudden cardiac death - usually due to a lethal cardiac arrhythmia – could be due to ischaemia impinging on the conduction system itself but usually due to electrical irritability of the myocardium away from the conduction system
• Chronic ischaemic heart disease - Usually used to describe patients who develop progressive cardiac failure as a result of ischaemic myocardial damage

Question 7

How does the gross morphology of the heart change during an MI?

Answer 7

1-2 days: The heart is pale, oedematous, myocyte necrosis and neutrophils

3-4 days: Yellow with haemorrhage edges, myocyte necrosis and macrophages

1-3 weeks: Red-grey to grey-white, pale, thin granulation tissue then fibrosis

3-6 weeks: Dense fibrous scar

Question 8

What are blood markers of cardiac myocyte damage?How else can you test for an MI?

Answer 8

• Troponin T&I - Detectable 2 – 3h, peaks at 12-48h, detectable to 7 days
  Raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
• Myoglobin - peak at 2h but also released from damaged skeletal muscle
• Lactate dehydrogenase isosenzyme 1 - peaks at 3 days, detectable to 14 days
• Aspartate transaminase - Also present in liver so less useful as a marker of myocardial damage
• Creatine Kinase MB

Clinical signs include: tachycardic, weak thread pulse, sweating, SOB, chest pain (radiating to jaw, left arm).

• 10%-15% are “silent” or atypical – much more common in women, elderly and those with diabetes
• ECG – cardiologists –ST elevation, new Q waves and other
• Investigations: ECG, cardiac enzymes, echo, angio

Question 9

What is the treatment for an MI?

Answer 9

Treatment:
M.O.N.A.: Morphine, Oxygen, Nitrates and Aspirin
Reperfusion: PCI (percutaneous coronary intervention); better than thrombolysis

The aim is to restore tissue perfusion as rapidly as possible to try to save ischaemic myocardium that is threatened by infarction. This may be done through:
• Thrombolysis (dissolving thrombus - this doesn’t affect underlying plaque)
• Balloon angioplasty (+/- stenting which eliminates occlusion and can relieve some of obstruction). A specially designed catheter with a tiny balloon is carefully guided through the artery to the blockage, then inflated to widen the opening and increase blood flow to the heart.
Coronary bypass grafting to allow flow around obstruction

Question 10

What is the prognosis of an MI?

Answer 10

Factors associated with poor prognosis – increasing age, female, DM, previous MI due to loss of functional myocardium). It still has a mortality rate of 35%.
• Of these deaths up to 70% are “sudden cardiac deaths” (within 1-2hrs)
• 10-15% early hospital mortality
• 7-10% further 1y mortality
3-4% mortality per year in subsequent years

Question 11

What are the complications of an MI?

Answer 11

• Arrhythmias (conduction disturbances and myocardial irritability)
• Ventricular fibrillation (LV dysfunction proportional to the size of the infarct) & sudden death
• Left ventricular failure & cardiogenic shock
• Myocardial rupture - tamponade, ventricular septal perforation (rare), papillary muscle(rare)

Further complications of MI
• Cardiac mural thrombus & emboli
• Ventricular aneurysm (true)
• Pericarditis - fibrinous or fibro haemorrhagic pericarditis usually develops at day 2-3 due to underlying myocardial inflammation
Others such as Dressler’s syndrome) +/- pleurisy, DVT & PE

Question 12

What is heart failure?

Answer 12

Heart failure, also known as congestive cardiac failure is a common result of many forms of heart disease. The heart unable to pump blood at the rate requires to meet the demands of the tissues.

Question 13

What is chronic IHD?

Answer 13

• Possibly result of previous (occult) MIs
• Congestive heart failure
• big heart, hypertrophied and dilated
Risk of sudden cardiac death or MI

Question 14

What are the symptoms and signs of IHD?

Answer 14

Patients with heart failure present with a variety of symptoms, most of which are nonspecific. The common symptoms of congestive heart failure include fatigue, dyspnoea, swollen ankles, and exercise intolerance, or symptoms that relate to the underlying cause. The accuracy of diagnosis by presenting clinical features alone, however, is often inadequate, particularly in women and elderly or obese patients.

Question 15

How is IHD managed?

Answer 15

Through drugs, vaccinations, surgery and lifestyle management.

Lifestyle: smoking cessation, alcohol reduction, exercise, weight loss, salt and fluid.

Surgery can be used to treat the cause (valve replacement, revascularisation etc.) and transplantation.

Question 16

What are the complications of IHD?

Answer 16

• Arrhythmias
• thromboembolism
• GI - hepatic congestion and dysfunction, malabsorption
• Musculoskeletal - muscle sting
• Respiratory - pulmonary congestion, resp. muscle weakness, pulmonary HTN (rare)

Question 17

What are the features of RHF?

Answer 17

RHF – usually occurs as a result of LHF but can be caused by severe pulmonary hypertension (cor pulmonale) when there is increased resistance in the pulmonary circulation. Hypertrophy and dilatation of the RV and engorgement of the systemic and portal venous systems (late) leading to hepatic and splenic enlargement, peripheral oedema, and ascites.

RHF leads to congestion of peripheral tissues. This can cause dependent oedema and ascites, GI congestion, anorexia, GI distress and weight loss) and liver congestion.

Question 18

What are the features of LHF?

Answer 18

LHF – progressive damming of blood within the pulmonary circulation. Leads to increased pressure leading to congestion and oedema and heavy wet lungs -> striking clinical symptoms (on call) – cough with sputum; breathlessness (exaggerated SOB on exertion), orthopnoea (2 pillows/sitting up), paroxysmal nocturnal dyspnoea (attacks of extreme SOB that wake the patient at night).

There is also impaired gas exchange leading to cyanosis and signs of hypoxia.

Decreased cardiac output leads to activity intolerance and signs of decreased tissue perfusion.