Coronary Insufficiency: Mechanisms, Effects, and Manifestations

Coronary Insufficiency: Definition and Determinants

Coronary Insufficiency: It is the disproportion between the amount of blood needed for the myocardium and the amount received. Myocardial perfusion depends on two coronary arteries originating from the aorta. Factors that increase myocardial O2 consumption include: tension developed by myocardial contraction, tachycardia, and increased contractility.

Coronary status is indirectly assessed via the ECG, exercise ECG, and stress echocardiogram, and directly through thallium scintigraphy to visualize coronary lesions where anatomical evidence exists.

Mechanisms and Causes

Decrease in Coronary Blood Flow

This decrease is often caused by atherosclerosis of the coronary arteries, which can be promoted by hypertension, dyslipidemia, diabetes, smoking, obesity, and a sedentary lifestyle. There may also be normal and pathological coronary spasms involving agents such as serotonin and vasoconstrictor thromboxane.

Increased O2 Needs

This occurs by increasing the tension developed by the ventricular wall, due to pressure overload from aortic valve disease or volume overload from intense physical exercise, etc. The following non-coronary causes can contribute to myocardial anoxia:

• Anemia
• Hypoxia
• CO poisoning
• Tachyarrhythmias
• Hypertensive crisis

Effect of Ischemic Myocardial Anoxia

Biochemical Impact

Biochemical disorders are responsible for the pain, the electrophysiological alterations, arrhythmias, and ECG changes.

Functional Effect

Contractile failure with decreased compliance contributes to decreased Cardiac Output (GC).

Myocardial Trophism

If ischemia is severe and prolonged, the affected area becomes necrotic, leading to a heart attack as a result.

Forms of Manifest Coronary Heart Disease

Angina Pectoris

This is an expression of transient coronary heart disease, characterized by pain and abnormal ECG findings. It must be emphasized if the pain is evident during effort. Facts that argue against the diagnosis of typical angina include:

• Pain location: apexianal, subxiphoid, infra-axillary, or fingertip.

Angina is classified according to its evolution as stable or unstable. Unstable angina is not considered due to increased O2 demand. An ECG is abnormal only during the crisis, characterized by ST segment depression in angina of effort and ST segment elevation at rest.

Myocardial Infarction

This is the result of severe, persistent, and localized coronary insufficiency, often caused by thrombosis related to stable atherosclerotic lesions or sustained spasms, leading to ischemic necrosis of an area of infarction. The pain is similar to angina but is more intense, prolonged, and is not relieved by rest or vasodilators. Sometimes the pain occurs at rest.

The hematological and biochemical changes that occur include:

• Leukocytosis with neutrophilia
• Increased alpha-globulin
• Increased body temperature

Complications: Heart failure and shock, arrhythmia, papillary muscle dysfunction and rupture, aneurysms, and post-MI pericarditis.

Sudden Death

A portion of sudden deaths occurs due to ventricular fibrillation triggered by coronary heart disease.