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Background The cause of severe cardiac conduction disturbances is often uncertain. The aim of this study was to examine a group of patients with permanent pacemakers who underwent coronary arteriography to determine the extent of coronary atherosclerotic disease that might be responsible for the conduction disturbances. Methods and Results Forty-three consecutive patients with a permanent pacemaker and 36 matched control patients were investigated. The coronary angiographic study included measurement of diameter and stenosis severity, qualitative assessment of flow, and classification of pathological anatomy, particularly the blood supply to territories supplying the different segments of the conduction system. Among 43 patients with a permanent pacemaker, 27 had ischemic heart disease (17 after coronary artery bypass graft surgery). The conduction disturbance was infranodal in 28 patients, sinus nodal in 6, AV nodal in 4, and complete AV block of unspecified origin in 5. Patients with permanent pacemakers had a coronary artery pathology compromising blood flow to the septal branches and the right coronary artery (type IV anatomy). This pattern was significantly different from the matched control patients, in whom the most prevalent coronary anatomy was the combination of right coronary artery with distal left anterior descending artery (not involving the septal branches) lesions ( P =.007). Conclusions Patients with coronary artery disease and severe conduction disturbances that require implantation of permanent pacemakers are more likely to have a specific pathological coronary anatomy that combines a compromised blood flow to the septal branches of the left anterior descending artery with right coronary artery lesions. The location of lesions in the coronary tree rather than severe diffuse atherosclerosis appears to be responsible for the conduction disturbances.

Thrombolytic therapy in acute myocardial infarction is of established value in recanalizing the occluded coronary artery, reducing infarct size, and decreasing mortality. Here, we review the extensive information provided by large clinical trials on agent and patient selection, timing of treatment, adjuvant therapies, and complications. Early treatment is of prime importance. Tissue plasminogen activator is slightly superior to streptokinase, especially in young patients treated early. Intravenous heparin should be used in conjunction with tissue plasminogen activator, although its role when streptokinase is used is less clear. Aspirin, beta-blockers, and converting enzyme inhibitors are of proven value as adjunctive therapies; nitrates and magnesium are not. Newer antithrombotic and antiplatelet agents (eg, hirudin and glycoprotein IIb/IIIa receptor antagonists) may further improve results.

BACKGROUND The coronary microvasculature may be abnormal even in the presence of angiographically normal epicardial arteries. Abnormalities of small coronary vessels have been invoked as a cause of angina. METHODS AND RESULTS To quantitatively evaluate the morphology of capillaries in patients with idiopathic dilated cardiomyopathy (DCM) or the syndrome of angina and small vessel disease (SVD), we performed electron microscopic morphometry of capillaries in right ventricular biopsy samples taken from 32 patients. Ten had angina, normal epicardial coronary arteries, and evidence for SVD; 12 had DCM; and 10 had normal hearts. In patients with DCM, the ratio of microvessels to myocytes was not different than that of controls (0.49 +/- 0.06 versus 0.51 +/- 0.05). Mean cross-sectional areas of the capillaries (lumen plus wall) and lumen were significantly greater than those of controls (45.3 +/- 15.1 versus 22.7 +/- 8.3 micron 2, p less than 0.001; 17.6 +/- 6.9 versus 11.6 +/- 6.2 micron 2, p less than 0.05, respectively). Fibrous content of the myocardium, as assessed by quantitative light microscopy, was significantly increased (16.3 +/- 3.3% versus 5.0 +/- 2.4%, p less than 0.001). In contrast, in patients with SVD, the capillary-to-myocyte ratio was reduced (0.33 +/- 0.08, p less than 0.001). Although mean cross-sectional areas of the entire capillary (32.4 +/- 19.7 micron 2) and the lumen (8.9 +/- 7.8 micron 2) were not statistically different than those of controls, there was an absence of capillaries less than 15 micron 2 in cross-sectional area, and the frequency distribution of the lumen area was skewed to the left. Swollen endothelial cells frequently encroached upon the lumen. There was a mild increase in fibrous content (9.5 +/- 3.7%, p less than 0.05). CONCLUSIONS Enlarged capillaries and a normal ratio of capillaries to myocytes appear to be features of DCM. Of the patients with SVD, there was both a relative lack of capillaries and capillary lumen narrowing from swollen endothelium. These changes may induce ischemia and angina and may result in mild fibrosis.