Life-threatening Dysrhythmias Research Articles

Right ventricular endomyocardial biopsy: Clinicopathologic correlates in 100 consecutive patients

The first 100 consecutive patients to undergo right ventricular endomyocardial biopsy at the Mayo Clinic were divided retrospectively into five groups, depending on the prebiopsy clinical diagnosis, and the biopsies were review histologically in a single-blind format. Group 1 consisted of 34 patients with a diagnosis of unexplained congestive heart failure and a dilated heart; of these, 4 (12%) had active myocarditis by biopsy. Of the six patients in group 2 with a clinical diagnosis of myocarditis, only one (17%) had biopsy evidence of inflammation, but two (33%) had changes that, in the clinical setting, were suggestive of cardiomyopathy. Group 3 consisted of 27 patients with dysrhythmia, syncope, or cardiac arrest but without congestive heart failure; of these, 4 (15%) had active myocarditis by biopsy, and 8 (30%) had changes that, with the clinical history, were consistent with cardiomyopathy. Group 4 included 19 patients with unexplained congestive heart failure and a nondilated heart; 4 (21%) had cardiac amyloid on biopsy. Group 5 was a diverse group of 14 patients with possible cardiac involvement by a known systemic disease; myocardial disease was documented by biopsy in 7 (50%). On the basis of these findings, we recommend endomyocardial biopsy (1) in patients with dilated cardiomyopathy in whom myocarditis is suspected, (2) in patients with the clinical diagnosis of active myocarditis in whom tissue documentation is indicated before treatment with anti-inflammatory or immunosuppressive drugs, (3) in patients with clinically unexplained life-threatening dysrhythmias in whom myocarditis or cardiomyopathy may be present, and (4) in patients with apparent hypertrophic or restrictive cardiomyopathy in whom cardiac amyloid may be present.

Postinfarction angina caused by coronary arterial spasm.

Recurrent ST-segment elevations in leads where new Q waves developed were repeatedly recorded in six patients during a recovery phase of acute myocardial infarction. Such ST-segment elevations were transient, occurred with or without chest pain, and returned to control levels. No enzymatic changes signifying recurrent myocardial necrosis were found after each episode. Selective coronary cineangiography in one patient demonstrated a mild segmental stenosis in the coronary artery perfusing the infarcted area; this artery became completely occluded after administration of i.v. ergonovine. Administration of calcium antagonists effectively reduced the frequency of postinfarction angina and ST-segment elevations. The clinical features suggest that the postinfarction angina in these patients is produced by coronary arterial spasm and that coronary arterial spasm may cause severe life-threatening dysrhythmias.

Surgical treatment of Wolff-Parkinson-White syndrome

Wolff-Parkinson-White (WPW) syndrome can be associated with disabling and life-threatening dysrhythmias that are resistant to medical treatment yet are amenable to surgical treatment. This report relates our experience with 10 Type A and 10 Type B patients who have been treated by surgery. The operation has evolved from one procedure, applicable to only a few patients, to a new procedure which allows the chance for cure for nearly all patients. By the old method, the Kent bundle was sectioned from the ventricular side; now it is divided from the atrial side, an approach which allows access to the septal tracts. There have been twelve cures, four partially successful operations, and four failures. In one failure, correction of a Type B lesion in the septal area was attempted via the old operation. In a second failure, WPW was associated with Ebstein's anomaly. In the other two failures, the Kent bundle entered the left side of the ventricular septum from the atrial septum at a point adjacent to the atrioventricular (AV) node and His bundle. This group, atrial septal Type A, may require His bundle division as well as Kent bundle division. All other patients with WPW can be cured by properly planned and performed operations.