Ischemic Heart Disease Overview

Ischemic Heart Disease

• Ischemic heart disease (IHD) involves several related syndromes caused by myocardial ischemia, an imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional needs.
• It's the leading cause of mortality worldwide, accounting for 7 million deaths annually.
• More than 90% of cases result from reduced coronary blood flow due to obstructive atherosclerosis.
• Less common causes include increased demand (e.g., heart rate or hypertension), diminished blood volume (e.g., hypotension or shock), diminished oxygenation (e.g., pneumonia), and reduced oxygen-carrying capacity (e.g., anemia or CO poisoning).

Angina Pectoris

• Angina pectoris is intermittent chest pain caused by transient, reversible myocardial ischemia.
• The pain is likely a consequence of ischemia-induced release of adenosine, bradykinin, and other molecules that stimulate autonomic afferents.
• Three types of angina are recognized:
• Typical or stable angina: episodic chest pain linked to exertion or increased demand (e.g., tachycardia). The pain is crushing or squeezing, radiating to the left arm or jaw. The pain is relieved by rest or nitroglycerin (a vasodilator).
• Prinzmetal or variant angina: occurs at rest and is caused by coronary artery spasms. Symptoms can be similar to typical angina, but can occur unexpectedly. It can affect normal vessels, not just those with existing plaques. Responds well to vasodilators.
• Unstable angina: characterized by increasingly frequent pain, precipitated by less exertion or even at rest. Often linked to plaque disruption, thrombosis, distal embolization, and/or vasospasm -- a precursor to myocardial infarction (MI).

Myocardial Infarction (MI)

• Also known as a "heart attack," MI involves necrosis (death) of heart muscle tissues due to ischemia.
• Atherosclerosis is the primary cause of MI, sharing the same risk factors.
• MI occurrences rise with age and increasing atherosclerosis.
• Approximately 10% occur before age 40, and 45% before age 65. Men are at higher risk than women initially, though the gap narrows with age.
• MI types include:
• Transmural infarction: involves the full thickness of the myocardium, usually due to coronary artery thrombosis.
• Subendocardial infarction: limited to the myocardium's inner third, usually due to transient decreases in oxygen delivery, increased oxygen demand, or when a thrombus lyses before complete infarction develops.
• Microscopic infarcts: occur in the setting of small-vessel occlusions, may not show significant ECG changes.

Clinical Features of MI

• Classic MI is typically associated with severe crushing, substernal chest pain that radiates to the neck, jaw, epigastrium, or left arm. Atypical symptoms can occur.
• Patients often present with a rapid, weak pulse, diaphoresis, weakness, lightheadedness, vomiting, and palpitations.
• Sometimes, cardiogenic shock might be present, which is marked by low blood pressure and fluid collection.

Electrocardiographic Abnormalities (ECG)

• ECG abnormalities, often including inverted T waves and deep Q waves, are common in MI.
• Arrhythmias are also frequent, potentially causing sudden cardiac death.

Laboratory Evaluation of MI

• Early MI indicators include rising CK-MB and troponin levels.
• CK-MB and activity peaks within 2-4 hours of MI, then returns to normal after approximately 72 hours, Absence of a significant change implies possible lack of MI.
• Troponins, typically not present in the bloodstream, rise within 2-4 hours of MI and remain elevated for days, providing a more precise and longer-term marker for the event.
• Absence of measurable changes in the first 2 days following chest pain often rules out MI as a diagnosis.

Consequences and Complications of MI

• Potential Complications include:
• Contractile dysfunction: some degree of left ventricular failure, manifested as low blood pressure, pulmonary congestion, and edema. Cardiogenic shock can occur.
• Right ventricular infarction: significant right-sided heart failure.
• Papillary muscle dysfunction: poorly contractile papillary muscles may result in post-infarct mitral regurgitation.
• Myocardial rupture (rare).
• Left ventricular wall rupture (rare).
• Ventricular septal rupture (rare).
• Arrhythmias (very common).
• Mural thrombus: occurs in combination with myocardial stasis and increased endocardial damage, potentially leading to thromboembolism.
• Pericarditis (inflammation around the heart): often occurs 2 to 3 days after MI.
• Ventricular aneurysm: a thinned, scar-tissue-filled section of a heart chamber, often after a large transmural infarct.

References - (These are not included to keep the summaries concise.)

• Robbins Basic Pathology (10th edition, by Vinay Kumar, Abul K. Abbas, and Jon C. Aster)