Ischemia in the territory of the first major septal perforator branch anomalously originating from the first diagonal branch leads to a transient leftward shift of the QRS axis in the frontal plane: a case report.

A patient with non-Q wave myocardial infarction had severe luminal narrowing in the first major septal perforator branch, which arose anomalously from the first diagonal branch. In this case, an exercise ECG showed a transient leftward QRS axis shift.

Myocardial infarction in a patient with severe aortic stenosis and normal coronary arteriograms: involvement of the circumferential subendocardial wall of the left ventricle.

A case of severe aortic stenosis with normal coronary arteriograms was associated with myocardial infarction involving the circumferential subendocardial wall of the left ventricle. The infarct was caused solely by the severe aortic stenosis and resulted from the extreme disparity between myocardial oxygen supply and demand.

Effect of cilostazol on the ventricular escape rate and neurohumoral factors in patients with third-degree atrioventricular block.

STUDY OBJECTIVES: This study assessed whether the antiplatelet agent cilostazol, which has potent cyclic nucleotide phosphodiesterase type-3 inhibitory activity, affects the ventricular escape rate and neurohumoral factors in patients with third-degree atrioventricular block. DESIGN: Prospective, but nonrandomized, study. SETTING: Cardiology division of an acute care hospital. PATIENTS: We studied 12 patients with third-degree intra-His or infra-His atrioventricular block who were in functional class II or III of the New York Heart Association classification. None of the patients had experienced Adams-Stokes attacks. INTERVENTIONS: These patients were given cilostazol orally at a dose of 200 mg daily for at least 1 week. MEASUREMENTS AND RESULTS: Before and after treatment with cilostazol, continuous 24-h ECG monitoring and measurement of plasma natriuretic peptide concentrations were performed. Cilostazol significantly increased the mean (+/- SEM) total 24-h QRS count from 57,300 +/- 2,800 to 74,400 +/- 3,200 beats (p = 0.001) and significantly decreased the maximum geometric mean R-R interval over a 24-h period from 1,900 ms (95% confidence interval [CI], 1,700 to 2,100 ms) to 1,600 ms (95% CI, 1,400 to 1,900 ms; p = 0.02), although none of the patients showed the abolishment of the atrioventricular conduction abnormalities. The total 24-h count of premature ventricular beats was not different before treatment (15 beats; 95% CI, 5 to 44 beats) and after treatment (12 beats; 95% CI, 5 to 30 beats; p = 0.57). Treatment with cilostazol significantly decreased the concentration of plasma atrial natriuretic peptide from 88 pg/mL (95% CI, 49 to 160 pg/mL) to 51 pg/mL (95% CI, 32 to 80 pg/mL; p = 0.007) and of brain natriuretic peptide from 166 pg/mL (95% CI, 71 to 389 pg/mL) to 77 pg/mL (95% CI, 30 to 178 pg/mL; p = 0.02). CONCLUSIONS: Cilostazol significantly increased the ventricular escape rate and significantly decreased the level of circulating natriuretic peptides. Thus, cilostazol could be safely given to selected patients over the short term with third-degree atrioventricular block.

Occurrence of transient U-wave inversion during vasospastic anginal attack is not related to the direction of concurrent ST-segment shift.

STUDY OBJECTIVES: We sought to assess the incidence of transient U-wave inversion during vasospasm of the left anterior descending coronary artery (LAD) with ST-segment depression as opposed to that with ST-segment elevation. DESIGN: Retrospective study. SETTING: Cardiology division of acute-care hospitals. PATIENTS: We studied 49 patients with vasospastic angina whose vasospasm was induced in the LAD, not in the left circumflex coronary artery, by intracoronary injection of acetylcholine. MEASUREMENTS AND RESULTS: The ECG traces obtained during acetylcholine-induced vasospasm of the LAD were examined. Based on the direction of ST-segment shift, the patients were categorized into two groups: the ST-segment elevation group (n = 27) and the depression group (n = 22). There were no differences in age, gender, or cardiovascular risk factors between the two groups. The distribution of the spastic site in the LAD was also similar. A total reduction in luminal diameter during a provoked attack was more often observed in the ST-segment elevation group than in the ST-segment depression group (37% vs 9%, p = 0.02). Collateral circulation to the LAD was found in only one patient in each group. There were no differences between the two groups in heart rate, systolic BP, and double product of heart rate and systolic BP during the attack. The incidence of acetylcholine-induced anginal attack with U-wave inversion in the ST-segment depression group was nearly as high as that in the ST-segment elevation group (77% vs 78%, p > 0.99). CONCLUSIONS: The development of transient U-wave inversion during vasospasm of the LAD induced by intracoronary injection of acetylcholine does not depend on the magnitude of myocardial ischemia as judged by the direction of ST-segment shift.