Sudden death due to valvular disease usually involves either mitral valve prolapse (floppy mitral valve; myxomatous degeneration of the mitral valve) or aortic stenosis. Rarely, sudden death will be due to an acute bacterial valvulitis (Figure 3.5). The valve involved is usually the tricuspid valve and the individual an intravenous drug abuser.
Until recently, it was estimated that 5-15% of the population had mitral valve prolapse. A study by Freed et al. of 1646 men and 1845 women, representing an unselected, community-based sample of ambulatory patients, and using current two-dimensional echocardiographic criteria, revealed an overall incidence of 2.4%.31 The mitral valve prolapse syndrome refers to a condition characterized by nonspecific symptoms (dyspnea, fatigue, dizziness, palpitation, anxiety, atypical chest pain), electrocardiographic abnormalities, and arrhythmias.31-33 The characteristic auscultation findings are midsystolic clicks and late systolic murmurs. The arrhythmias are widely varied, with premature ventricular complexes being the most prevalent. The anatomical findings are voluminous, thickened, redundant valve leaflets showing myxomatous transformation of the valve substance, in the absence of any inflammatory change, and dilatation of the mitral annulus (Figure 3.6). The posterior leaflet of the mitral valve is allegedly involved more than the anterior, though this has not been the authors' impression.
Clinically, there is protrusion of the mitral leaflets into the left atrium during systole. Complications of mitral valve prolapse are sudden death due to ventricular fibrillation, infective endocarditis, transient ischemic attacks and partial strokes secondary to clot or platelet aggregations originating from the prolapsed valve, ruptured chordae tendinae, and progression to mitral insufficiency.31-32
Deaths due to mitral valve prolapse are uncommon. Diagnosis of this entity as a cause of death is made by exclusion. One would have to do a complete autopsy, including a thorough toxicological screen, to exclude other possible causes of death before making the diagnosis. In the cases the authors have seen, the myxomatous degeneration of the valves has been extremely marked and has involved both leaflets of the mitral valve. The victims have generally been female, with the youngest 12 years of age and the rest in their late teens, twenties, and early thirties. Some have had a previous history of arrhythmias. One 18-year-old girl, who had been on propranolol for her arrhythmias, had her medication stopped approximately a month before collapsing and dying in front of a number of witnesses.
After mitral valve prolapse, the next most common cause of sudden death due to valvular disease is aortic stenosis (Figure 3.7). Mitral stenosis, once a common finding in the medical examiner's office, has almost disappeared due to the marked decline in rheumatic fever and the surgical treatment for mitral stenosis. Aortic stenosis may have four etiological causes: congenital malformation of the valve, rheumatic inflammation with fusion of the cusps, secondary calcification of congenital bicuspid valves, and primary degenerative calcification of normal aortic valves.34Congenital aortic stenosis, which excludes the bicuspic aortic valve, refers to conditions present at the time of birth. Congenital stenotic valves will develop secondary calcification as the individual gets older. This condition is rarely seen in the medical examiner's office because diagnosis has usually been made and treatment administered.
Rheumatic aortic stenosis is becoming uncommon for the same reason that mitral stenosis is uncommon — the relative absence of rheumatic fever in the population. In rheumatic aortic stenosis, there is fusion of the cusps due to the inflammatory process. Calcification develops in patients as they grow older, generally over the age of 40.
In both secondary calcification of the bicuspid valves and primary degenerative calcification of the normal aortic valve, it is the calcium deposit that is the principal cause of the stenosis. With the bicuspid aortic valves, calcification begins in the 6th, 7th, and 8th decades of life, developing at the free
Figure 3.7 Aortic stenosis.
edges of the cusps and progressing toward the base. In primary degenerative calcification of normal aortic valves, the calcification progresses from the base toward the edges and usually involves individuals in the 8th and 9th decade of life.
At the present time, the most common cause of aortic stenosis is calcification of bicuspid valves. It should be noted that bicuspid aortic valves, the precursor of calcific aortic stenosis, are present in approximately 0.4% of the population.
The aspect of aortic stenosis of most interest to the forensic pathologist is the propensity for sudden death. The mechanism of death is presumably acute myocardial insufficiency secondary to obstruction of the left ventricular outflow. The most disturbing case that the authors have seen with calcific aortic stenosis was that of a commercial airplane pilot in his late forties who collapsed and died while jogging. This condition apparently was not detected in any of his physical examinations.
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