Sudden coronary death. Frequency of active coronary lesions, inactive coronary lesions, and myocardial infarction.

BACKGROUND: The reported frequency of active coronary lesions (plaque rupture and coronary thrombosis) in sudden death due to coronary artery atherosclerosis (sudden coronary death) has varied from < 20% to > 80% of cases in previous series. In hearts lacking an active coronary lesion, sudden death has usually been attributed to a healed myocardial infarction. The purpose of the present study was to determine the frequency of active and inactive coronary lesions and myocardial infarction in individuals with sudden coronary death. METHODS AND RESULTS: The hearts of persons who died as a result of sudden coronary death underwent perfusion-fixation and postmortem angiography. An active coronary lesion was defined as a disrupted plaque, luminal fibrin/platelet thrombus, or both. We defined an inactive lesion as having a cross-sectional luminal stenosis of > or = 75% with neither plaque disruption nor luminal thrombus. Ninety hearts were examined (from 72 men and 18 women; mean age at the time of death, 51 +/- 10 years). Acute myocardial infarction was present in 19 (21% [acute myocardial infarction only in 9, both acute and healed myocardial infarction in 10]), healed myocardial infarction only in 37 (41%), and no myocardial infarction in 34 (38%). Active coronary lesions were identified in 51 (57%): acute thrombi plus disrupted plaques in 27, acute thrombi only in 21, and disrupted plaques only in 3. In hearts with acute myocardial infarction, active coronary lesions were significantly more prevalent than in hearts with only healed myocardial infarction or hearts lacking an acute or a healed myocardial infarction (89%, 46%, and 50%, respectively; P < .005). Hearts without acute or healed myocardial infarction and without active lesions were similar to hearts with active lesions with respect to heart weight and severity of epicardial coronary disease. CONCLUSIONS: Acute changes in coronary plaque morphology (thrombus, plaque disruption, or both) were found in 57% of cases of sudden coronary death. In hearts with myocardial scars and no acute infarction, active coronary lesions were identified in 46% of cases. Neither myocardial infarction (acute or healed) nor an active coronary lesion was present in 19% of hearts.

Causes of sudden cardiac death in patients with replacement valves: an autopsy study.

We retrospectively reviewed 52 hearts from patients who had heart valve replacement more than one month prior to death. In 37 cases death was sudden (less than 6 hours after symptoms). These 37 cases were divided as Group I (15 cases, sudden death related to valve prosthesis); and Group II (22 patients, sudden death not related to valve prosthesis). Causes of death in Group I were valve thrombosis (n = 4), embolization of valve thrombi (n = 2), strut fracture (n = 2), anticoagulation-related hemorrhage (n = 2), perivalvular fistula (n = 1) and left ventricular outflow obstruction (n = 1). Causes of death in Group II were presumed arrhythmia in 14, myocardial infarction in six and aortic rupture in two cases. Severe coronary atherosclerosis (> 75% cross-sectional area luminal narrowing) was present in five of 14 cases dying of arrhythmia and in all six cases with myocardial infarction; in the remaining cases, there was marked cardiac hypertrophy (mean weight 728 +/- 177 grams). The mean age (54 +/- 18 vs. 54 +/- 13 years, respectively) was similar in both groups. Seven of 21 deaths after aortic, 6/12 deaths after mitral, 10/25 deaths after mechanical, and 5/11 after porcine valve replacement were secondary to valve complications. The mean left ventricular thickness was 1.7 cm in both groups, the mean left ventricular cavity dimension 2.8 +/- 1.4 cm in Group I vs. 3.5 +/- 1.4 cm in Group II, and the mean heart weight was 550 grams in Group I vs. 734 +/- 211 in Group II (p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemoperfusion in theophylline neurotoxicity.

Four patients with severe theophylline toxicity (theophylline levels of 60 to 180 micrograms/ml) are reported. Three patients with neurotoxicity were treated with hemoperfusion. Two of these were hemoperfused early after the onset of seizures; they recovered with no neurologic deficit. In the third patient hemoperfusion was delayed for 16 hours after uncontrolled seizures; severe brain damage resulted. The fourth patient, who had the highest peak theophylline level but no seizures, was successfully treated with conservative management and peritoneal dialysis. The role of hemoperfusion in severe theophylline intoxication is discussed.