Stunned Myocardium
PKGhatak, MD
Coronary arterial occlusion causes chest pain and demands an immediate ER visit. Often family members are told it is a heart attack or myocardial infarction using a medical term. Not all coronary occlusions result in infarctions thanks to timely angioplasty, thrombolytic therapy, or having only partial obstruction of circulation. Immediately after a successful full restoration of circulation the cardiac enzymes and ECG return to normal. However, an echocardiogram may show a decrease in the contractile function of ventricles and the ejection fraction (EF) less than normal (75 – 55 %). Serial studies show a remarkable improvement of EF in the next 2 days, then a slow improvement over several weeks. Dr. Braunwald and Kolner in 1982 described this condition and called it Stunned Myocardium. However, years earlier Dr. Heydrickx showed, in experimental dogs by occluding coronary circulation temporarily for 2 to 15 minutes followed by full restoration of blood flow, decreased myocardial contractually but his peers did not believe this experiment and rejected his paper submitted for publication.
Difficulties in studying the living human heart.
Stunned myocardium is a functional abnormality of the heart muscles and is reversible. Changes in heart muscles do not faithfully reflect changes seen in blood and require the study of heart muscle cells. Biopsy of the heart for a reversible disease is out of the question. Experiments are carried out on dogs and pigs for that purpose. The metabolic paths, cytokines and sympathetic control of the human heart are different from animals. And not all that is known from animal studies is applicable to humans.
Cause of stunned myocardium.
The precise reason is still debated even today. High energy ATP (adenosine triphosphate) generation, the sympathetic neural response is delayed or deficient. ACE (angiotensin I enzyme), bradykinin, and prostacyclin actions on the myocardium are complex. Restoration of circulation restores the oxygen supply to the myocardium, which generated free radicals that break down contractile protein troponin I and paradoxically depresses myocardial contractility further. The use of Superoxide Dismutase, an inactivating agent, improves stunned myocardium. In stunned myocardium the Mitochondrial electron transfer is delayed, oxidation of catecholamines depresses contraction, ATP derived energy generation is suppressed, action potential generation is prolonged, energy dependent on calcium channels interfere with calcium ion movements and calcium overload of the sarcoplasmic reticulum and myocardium results in depressed contractility. Prophylactic use of calcium channel blockers prevents stunned myocardium.
ACE, bradykinin and prostacyclin.
An increase in ACE activity increases angiotensin I and bradykinin. Angiotensin II is a potent vasoconstrictor and positive inotrope results in increased ischemia. On the other hand, an increase in bradykinins generates more prostacyclin and nitrous oxide (NO) both are known to minimize stunning.
Clinical situation producing stunning.
Cardiac surgery. During inflating a deflating balloon at the time of angioplasty. Cardiac stress test in chronic angina. Emotional stress. Dialysis.
Hibernating myocardium.
Decreased myocardial contractility over a longer period of time from chronic coronary disease or repeated stunned myocardium is known as hibernating myocardium. The myocardial cells are viable but require weeks or months to return to normal function.
Takotsubo cardiomyopathy.
This is another example of myocardial wall motion abnormality in temporary myocardial ischemia. Patients are postmenopausal women subjected to severe mental stress prior to the development of chest pain and shortness of breath. ST-T is elevated in ECG and also cardiac enzymes are elevated. However, the Coronary angiogram shows no abnormality. An echocardiogram reveals Left ventricular apical ballooning but a normal wall motion of the base of ventricles is an indication of more than a single coronary artery spasm. The excised myocardiocytes show vacuoles filled with lipids, damaged mitochondria, edema and mononuclear cell infiltration, local necrosis and fibrosis. Patients usually fully recover in 2 to 5 weeks.
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