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Myocardial and Pericardial Disease: Difference between revisions
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Myocardial and Pericardial Disease (view source)
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==== Secondary cardiomyopathies ==== | ==== Secondary cardiomyopathies ==== | ||
Nine different subgroups of secondary myocardial disease exist, which are defined as diseases of the myocardium with a known cause. | Nine different subgroups of secondary myocardial disease exist, which are defined as diseases of the myocardium with a known cause. | ||
== Secondary myocardial disease == | |||
Myocardial disease with a known origin is termed secondary myocardial disease. Timely correction of the originating disease may result in reversal of the cardiomyopathy. Nine different etiologies can be distinguished: | |||
* Hypertension | |||
* Ischaemia | |||
* Valvular disease | |||
* Alcohol | |||
* Metabolic cardiomyopathy | |||
* Takotsubo cardiomyopathy | |||
* Peripartum cardiomyopathy | |||
* Tachycardia | |||
* Muscular dystrophy | |||
=== Hypertension or valvular disease === | |||
Inadequately treated hypertension or aortic stenosis results in adaptation of the left ventricle by means of hypertrophy. Although primarily considered an adaptive process to systolic overload, hypertrophy of the left ventricle is associated with ventricular dysfunction, arrhythmias, and sudden cardiac death. The process of hypertrophy involves enlargement and proliferation of myocytes, and interstitial fibrosis characterized by deposition of collagen type I and III. With increasing fibrosis, the compliance of the ventricle decreases resulting in loss of diastolic function before systolic function is impaired. Within this process of increasing myocardial mass, the coronary vasculature fails to adapt accordingly. To compensate, the auto-regulatory mechanisms exhaust part of the coronary reserve by decreasing vascular resistance during resting conditions by vasodilation, to accommodate to the increase in myocardial oxygen demand. This renders the myocardium at high risk for ischemia, and hence, patients may suffer from anginal complaints even in the absence of significant coronary artery disease. In patients with LVH, atrial fibrillation and ventricular arrhythmias, including multifocal ventricular extrasystoles, and short runs of ventricular tachycardia, are frequently found. The combination of myocardial fibrosis, maladaptation of the vasculature causing ischemia, autonomic imbalance and a prolongation of the action potential may serve as arrhythmogenic substrate in patients with LVH, resulting in an increased risk of sudden cardiac death. | |||
Adequate antihypertensive treatment, with ACE inhibitors and angiotensine receptor antagonist shown to be most potent, results in a regression of left ventricular mass. Calcium antagonists were also shown to result in LV mass regression, but importantly atenolol has been linked with a controversial increase in cardiovascular mortality in patients with LVH. In patients with aortic stenosis, infinite treatment is valvular replacement to relief the systolic overload of the ventricle. | |||
With regression of the ventricle, improved diastolic, and preserved systolic function result, as well as a relief of vascular maladaptation-induced ischemia. The combination of which results in a decrease in cardiovascular events. | |||
=== Ischemic cardiomyopathy === | |||
==== Alcohol ==== | |||
Long-term alcohol abuse, >80g of alcohol per day (equivalent to 1 liter of wine) for more than 5 years, may lead to a dilated form of cardiomyopathy. Alcohol-induced dilated cardiomyopathy is the leading cause of non-ischemic dilated cardiomyopathy, accounting for approximately 50% of cases. Most probably genetic predisposition for DCM plays an important role, as excess alcohol consumptions prevails far more often than alcoholic cardiomyopathy (ACM). Both the direct toxic effects of ethanol and its metabolites, as well as frequently occurring concomitant deficiencies of vitamins, minerals or electrolytes may adversely affect myocardial function (TABLE). | |||