| Abstract: | ![]()
The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following: 1. The posterior papillary muscle was almost completely separated from its base, with only a thin strip of muscle intact. The mitral valve thus was insufficient (a “flail valve“); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray. 2. Cardiac hypertrophy (weight = 561 g) was undoubtedly the result of the increased workload imposed on the left ventricle by the systemic arterial hypertension that this patient had for several years. A high blood pressure that persists after a myocardial infarct predisposes to myocardial rupture, but was probably not a risk factor in her case since it did not persist. 3. The cause of the myocardial infarct was the thrombotic occlusion of the right coronary artery (on top of severe three-vessel coronary atherosclerosis), which resulted in infarction of the right as well as the posterior left ventricle and can partly explain the mistaken clinical impression that she had pulmonary emboli. |
