HEART DISEASESManar hajeer, MD

University of Jordan

Faculty of medicine, pathology department.

LEFT-SIDED HEART FAILURE

Causes:

a. Ischemic heart disease (IHD),

b. Systemic hypertension,

c. Mitral or aortic valve disease.

d. Diseases of myocardium.

CLINICAL FEATURES

a. Dyspnea on exertion is the earliest and most significant symptom.

b. Cough.

c. Orthopnea: Dyspnea when recumbent occurs because the supine position increases venous return from the lower extremities and typically is relieved by sitting or standing,

d. Paroxysmal nocturnal dyspnea : dyspnea awakening patients from sleep with feelings of suffocation.

e. Fine rales at the lung bases, caused by pulmonary edema.

f. Diminished cardiac output leads to decreased renal perfusion and diminished cerebral perfusion

II. RIGHT-SIDED HEART FAILURE

Usually is the consequence of left-sided heart failure. Causes of isolated right-sided heart failurea. Severe pulmonary hypertension resulting in right-sided heart

failure (cor pulmonale). b. Pulmonic or tricuspid valve disease.c. Congenital left-to-right shunts.

CLINICAL FEATURES

Related to systemic and portal venous congestion including congestive hepatomegaly and splenomegaly, peripheral edema (ankle and pretibial) , pleural and pericardial effusion and ascites.

In chronic cardiac decompensation, patients present with biventricular CHF encompassing syndromes of both right-sided and left-sided heart failure.

III. ISCHEMIC HEART DISEASE)(IHD)

- An imbalance between cardiac oxygen supply and myocardial demand.

- Called coronary artery disease (CAD)..- In more than 90% of cases, IHD is due to reduced coronary

blood flow secondary to obstructive atherosclerosis

THE CLINICAL PRESENTATION

I. Angina Pectoris : Is an intermittent chest pain caused by transient, reversible

myocardial ischemia.

II. Myocardial infarction.

III. Chronic ischemic heart disease.

IV. Sudden cardiac death.

ANGINA VARIANTS

a. Typical or stable angina

is episodic chest pain associated with exertion or tachycardia and the pain is a crushing or squeezing substernal sensation, that can radiate to left arm or to the left jaw (referred pain) and usually is relieved by rest or by drugs (nitroglycerin: a vasodilator that increases coronary perfusion).

- Is caused by fixed atherosclerotic lesion that occlude more than 70% of a coronary vessel.

b. Prinzmetal or variant angina :

Might be caused by vasospasm.

c. Unstable angina:

- Called crescendo angina, it occurs at rest

- Caused by fixed atherosclerotic lesion that occludes 90% of vessel lumen.

- It is often the harbinger of MI.

MYOCARDIAL INFARCTION (MI),

Referred to as "heart attack,“ and means necrosis of heart muscle resulting from ischemia.

- MIs can occur at virtually any age but the frequency rises progressively with increasing age.

- Approximately 10% of MIs occur before age 40.

- Men are at significantly greater risk than women, and women tend to be protected against MI during their reproductive years.

- However, menopause women with declining estrogen is associated with exacerbation of coronary artery disease and IHD is the most common cause of death in elderly women

PATHOGENESIS OF MI:

1. Caused by completely obstructive thrombus over a disrupted atheroclerotic plaque (can cause a massive MI).

- Influences extrinsic to plaque are important.- Adrenergic stimulation put physical stress on the

plaque by causing hypertension or vasospasm.- Surge in adrenergic stimulation associated with

awakening and rising may underlie that the incidence of acute MI is highest in early morning.

2. In 10% of MI infarction occurs in the absence of occlusive atherosclerosis and such infarcts are mostly attributable to coronary artery vasospasm.

In a typical MI, within minutes, the thrombus evolve to completely occlude the coronary artery lumen.

Angiography performed within 4 hours of the onset of

MI demonstrates coronary thrombosis in almost 90% of cases .

When angiography is performed 12 to 24 hours after onset of symptoms, evidence of thrombosis is seen in only 60% of patients, even without intervention, due to fibrinolysis.

Early thrombolysis can be successful in limiting the extent of myocardial necrosis

THE SEQUENCE OF CHANGES IN MI:

1. Loss of contractility occurs within a minute of onset of ischemia and may be reversible.

2. Myocyte coagulative necrosis, in severe ischemia lasting 20 to 40 minutes.

Thus, if, myocardial blood flow is restored before irreversible injury ,cell viability can be preserved; and this is the rationale for early diagnosis of MI and intervention.

3. In the postischemic state, myocardium remains profoundly dysfunctional for at least several days caused by persistent abnormalities in cell biochemistry that result in a non- contractile state (called stunned myocardium) and it can produce reversible cardiac failure

4. Although massive myocardial damage can cause fatal mechanical failure, in 80% to 90% of the cases , the death is due to ventricular fibrillation

ATHEROSCLEROTIC NARROWING CAN AFFECT:

1. Left anterior descending (LAD), 2. Left circumflex (LCX), 3. Right coronary artery (RCA)

Clinically significant plaques tend to occur within the first several centimeters of the LAD and LCX, and along the entire length of the RCA.

The location, size, and morphologic features of an acute MI depend on:

1.The size and distribution of the involved vessel.

2. The rate of development and the duration of the occlusion.

3. Extent of collateral supply.

COLLATERAL SUPPLY

- If an atherosclerotic lesion progressively occludes a coronary artery at slow rate over years, this causes remodelling of other coronary vessels which may provide compensatory blood flow.

- Such collateral perfusion can protect against MI even if the vessel eventually becomes completely occluded (alternative way for flow).

- These collaterals normally are closed, gradual narrowing of one artery allows blood to flow from high to low pressure areas through the collaterals, therefore; gradual collateral dilation can provide adequate perfusion to myocardium.

- With acute coronary blockage, there is no time for collateral flow to develop and infarction results.

SUBTYPES OF MI.

1. Transmural infarctions: Involve > 50% of the myocardial wall thickness.

2. Subendocardial infarctions : limited to the inner third of the myocardium.

CLINICAL FEATURES

a. Severe crushing substernal chest pain that can radiate to the neck, epigastria, jaw or left arm.

- In 10% to 15%, MIs may even be "silent" infarcts (particularly common in patients with diabetes mellitus)

b. Rapid and weak pulse.

c. Nausea and sweating.

d. Dyspnea attributable to resultant acute pulmonary edema.

THE LABORATORY EVALUATION OF MI

- Based on measuring blood levels of macro -molecules that leak out of injured myocardial cells

- Cardiac troponins and CK-MB have high specificity and sensitivity for MI

- CK-MB remains a valuable marker of myocardial injury, second only to the cardiac-specific troponins.

Total CK activity is not a reliable marker of cardiac injury since various isoforms of CK are found in brain and skeletal muscle.

- CK-MB isoform is the more specific indicator of heart damage and its activity begins to rise within 2 to 4 hours of MI, peaks at 24 to 48 hours, and returns to normal within 72 hours.

- TnI and TnT normally are not found in the circulation; however, after acute MI, both are detectable within 2 to 4 hours, with levels peaking at 48 hours and remaining elevated for 7 to 10 days.

- Both are sensitive markers for the early stages of an MI. However, persistence of elevated troponin levels for approximately 10 days allows the diagnosis of an acute MI long after CK-MB levels have returned to normal

COMPLICATIONS OF MYOCARDIAL INFARCTION

Occur in Nearly three fourths of patients

1. Contractile dysfunction: In most cases of MI, there is some degree of left ventricular failure.

2. Cardiogenic shock due to pump failure occurs in 10% of patients with MIs and typically is associated with infarcts that damage 40% of the left ventricle.

3. Papillary muscle dysfunction leads to post-infarct mitral regurgitation. It can result from post infarct ischemic dysfunction and later from muscle fibrosis and shortening .

4. Myocardial rupture:complicates 1% to 5% of MIs but is fatal when it occurs.

Left ventricular free wall rupture is the most common, usually resulting in rapidly fatal hemopericardium and cardiac tamponade.

- It occurs commonly within 3 to 7 days after infarction especially in females and age older than 60 years.

- Other risk factors include anterior or lateral wall infarctions, and first MI (as scarring associated with prior MIs tends to limit the risk of myocardial tearing).

5. Arrhythmias: due to myocardial irritability and conduction disturbances that can cause sudden death

- Approximately 90% of patients develop some form of rhythm disturbance,

The risk of ventricular fibrillation is greatest in the first hour and declines thereafter.

6. Pericarditis. : manifested as anterior chest pain and a pericardial friction rub and appears 2 to 3 days after infarction . Severe pericardial inflammation can lead to fibrosis to form dense adhesions that manifest as a constrictive lesion.

7. Mural thrombus: Due to combination of stasis and endocardial damage.

8.Ventricular aneurysm: is a late complication, and most commonly result from a large anteroseptal infarct that heals with the formation a thinned wall of scar tissue and usually do not rupture (since fibrotic)

9. Progressive late heart failure.