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Biomedical subjects

S Maybaum

Publications and source records attributed to S Maybaum.

5 recordsLinked to original sources
PubMed2000

Acute type 5 phosphodiesterase inhibition with sildenafil enhances flow-mediated vasodilation in patients with chronic heart failure.

OBJECTIVES: To determine the acute effects of type 5 phosphodiesterase inhibition with sildenafil on flow-mediated vasodilation in the brachial artery of patients with chronic heart failure. BACKGROUND: Impaired endothelium-dependent, flow-mediated vasodilation in patients with heart failure is partly attributable to hyporesponsiveness of cyclic guanosine monophosphate (cGMP) mediated vasorelaxation effector mechanisms in vascular smooth muscle. The effect of inhibition of cGMP degradation with sildenafil, a specific type 5 cGMP phosphodiesterase inhibitor, on flow-mediated dilation in heart failure is unknown. METHODS: Flow-mediated vasodilation after release of 1, 3 and 5 min of transient arterial occlusion was measured in the brachial artery with high resolution two-dimensional ultrasound imaging in 48 patients with chronic heart failure before and 1 h after randomized, double-blind assignment to a single oral dose of sildenafil 12.5, 25 or 50 mg or matching placebo. RESULTS: In response to oral administration of a single dose of study drug, the change in flow-mediated vasodilation after release of 1, 3 and 5 min of arterial occlusion was significantly greater in patients receiving sildenafil 25 mg (3.3 +/- 1.9, 3.8 +/- 1.8 and 4.0 +/- 1.8%, respectively, p < 0.05) and patients receiving sildenafil 50 mg (3.7 +/- 1.3, 4.1 +/- 1.1, 3.9 +/- 1.3%, respectively, p < 0.05) than that of patients receiving placebo (0.7 +/- 1.1, 0.2 +/- 1.2, 0.6 +/- 0.8%, respectively). CONCLUSIONS: Acute type 5 phosphodiesterase inhibition with sildenafil 25 and 50 mg increases endothelium-dependent, flow-mediated vasodilation in patients with chronic heart failure when compared with placebo.

Blood Circulation↗
PubMed1997

Attenuation of severity of myocardial ischemia during repeated daily ischemic episodes.

OBJECTIVES: The purpose of this study was to assess whether the severity of myocardial ischemia would be attenuated by repeated daily ischemic episodes, recorded by ambulatory electrocardiographic monitoring (AEM). BACKGROUND: Repetitive ischemic episodes induced by brief coronary occlusions in animal experiments and in humans during balloon coronary angioplasty produce preconditioning. We wanted to assess whether this phenomenon also exists during daily ischemic episodes. METHODS: Twenty-one patients with known coronary artery disease and ischemia on exercise testing and AEM were requested to walk a distance known to have previously caused myocardial ischemia on three consecutive occasions. Walking time was approximately 15 min and was followed by 5 min of rest. RESULTS: Mean maximal heart rate during the three walks was similar; however, the mean maximal ST segment depression decreased significantly from 2.21 mm during the first walk to 1.61 mm and 1.43 mm, respectively, on the second and third walks (p = 0.001). Ischemia duration was also significantly reduced on the second and third walks by 56% from 514 to 228 and 254 s, respectively (p = 0.012). The heart rate at onset of ischemia (ischemic threshold) increased from 99 beats/min on the first walk to 101 beats/min on the second walk and to 106 beats/min on the third walk (p = 0.058). CONCLUSIONS: This study demonstrated attenuation of myocardial ischemia with an associated increase in ischemic threshold in patients with repeated and adjacent ischemic episodes. This form of myocardial protection is likely to be encountered in patients during ordinary activity and may represent the clinical counterpart of myocardial preconditioning.

Coronary Disease↗
PubMed1996

Improvement in ischemic parameters during repeated exercise testing: a possible model for myocardial preconditioning.

Repeated short episodes of coronary occlusion in experimental animals, and in humans during balloon angioplasty, cause myocardial preconditioning. This study examines whether myocardial ischemia induced by repeated exercise testing can reduce the extent of ischemia induced by subsequent exercise tests. Twenty-six patients with positive stress tests underwent 3 treadmill exercise tests at 30-minute intervals. Two additional tests were performed on each of the previous 2 days in order to eliminate and/or reduce the training effect. All 3 exercise tests were of similar work load. In spite of that, total ischemic time was markedly shortened from 633 to 399 seconds (p <0.0001) as well as the recovery time from 259 to 126 seconds (p <0.0001) between the first and the second tests. There was no further improvement on the third test. Time to 1-mm ST depression was prolonged from 487 to 593 seconds (p = 0.004) and double product at 1-mm ST depression was increased in the second test from 20,322 to 22,325 mm Hg/second (p = 0.008), implying a higher ischemic threshold. An improvement of > or = 10% in < or = 1 ischemic parameter was observed in 25 of the 26 patients and in > or = 2 of the ischemic parameters in 76% of the patients. Improvement in ischemic parameters develops during repeated exercise induced ischemia in most patients. We suggest that this phenomenon, which was previously known as "warm up," is the clinical counterpart of myocardial preconditioning which develops not only during ischemia caused by reduction in coronary flow, but also during demand-induced ischemia.

Coronary Angiography↗