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Biomedical subjects

W H Herbert

Publications and source records attributed to W H Herbert.

At least 19 recordsLinked to original sources

Left bundle branch block and coronary artery disease.

This study tries the concept that left bundle-branch block (LBBB) connotes coronary artery disease (CAD). The findings indicate that prior studies both supporting of and in contradiction to the premise of a positive correlation have been biased by pre-selection of the patients reviewed. The data indicate, therefore, that LBBB is related to multiple entities. The major categories are CAD and/or hypertension myocardiopathy and aortic valvular disease. In addition, LBBB may develop during the acute phase of myocardial infarction. Its existence as a wholly benign entity has been documented as well. Further, this study adds still another group with LBBB. Six of the nine LBBB patients were female. Five of these, in spite of typical anginal histories, had no arteriographically demonstrable CAD. The absence of disease was surprising and the incidence of women with LBBB was greater than anticipated, thus providing some basis for suggesting that these women may be representative of still another group with LBBB. Further, this study supports the findings of Lewis et al by confirming an association between LBBB and a statistically shorter LCA mainstem (p less than 0.001).

Adult

Cigarette smoking and arteriographically demonstrable coronary artery disease.

Patients undergoing selective coronary arteriography were studied to determine whether the extend of their coronary artery disease (CAD) was related to cigarette consumption. Those without demonstrable lesions averaged 29.0 pack years. Patients with single vessel disease, 38.3 pack years, those with double vessel disease 44.9 pack years and those with triple vessel disease 67.5 pack years. Nonsmokers with significant CAD were ten years older than their smoking counterparts (p less than 0.01). Forty-seven percent of patients with no demonstrable disease were nonsmokers whereas only 18 percnet of those with CAD were nonsmokers (p less than 0.001). Sixty-nine percent of nonsmoking normotensive patients had no CAD whereas only 23 percent of nonsmoking hypertensive patients fell in the no CAD category (p=0.01-0.005). This study demonstrates a correlation between the number of cigarettes consumed and the severity of CAD as well as the accelerating effect of cigarette consumption on the development of CAD. It also suggests that symptomatic CAD in a normotensive nonsmoker is unusual.

Adult