Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart rate (HR), cardiac output (CO), coronary sinus blood flow (CSF), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), mean arterial (MAP), and coronary arteriovenous difference for oxygen (AVDcO2) were measured in patients with stable angina pectoris without cardiac failure before and 40 to 60 minutes after administration of 2 or 3 mg of molsidomine. In 20 patients these measurements were made in basal state during spontaneous rhythm. In eight of these patients (including three receiving beta blockers) the measurements were made during atrial pacing. In eight other patients, all receiving long-term beta-blocker therapy, the measurements were made during cold pressor test. At the basal state in spontaneous rhythm, a gradual reduction in the LVSP to 70% or less of its initial value was observed in four patients receiving 3 mg of molsidomine (two of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In the 16 other patients molsidomine decreased LVSP, LVEDP, MAP, CO, and double product (DP = LVSP X HR). The AVDcO2 was unchanged. CSF and myocardial oxygen uptake index (MVO2 = CSF X AVDcO2) were decreased. During atrial pacing, hemodynamic and coronary effects were similar to those seen in the basal state. During the cold pressor test, the increases in LVSP, MAP, and LVEDP were significantly reduced by molsidomine. The variations in CSF and coronary resistance (MAP/CSF) were also significantly different after administration of molsidomine, with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and coronary effects of molsidomine at basal state, during atrial pacing, and during cold pressor test in patients with stable angina pectoris. 383 4

The electrophysiological and mechanical events that follow transient therapeutic coronary artery balloon occlusion were analyzed in five patients. A marked (mean, 60 msec) decrease in the repolarization time of the left ventricular ischemic zone (assessed indirectly from endocardial monophasic action potential [MAP] recordings) ensued within 6 to 10 beats of occlusion. Abnormalities in left ventricular relaxation occurred almost simultaneously and preceded contraction abnormalities. A shift in the ST segment in the electrocardiogram (ECG) usually followed within the next 5 to 10 beats. An increase in heart rate (approximately 10 beats per minute) appeared last in the sequence of events. Angina was a variable parameter, frequently absent. Thus, intracavitary recordings of the electrical and mechanical changes are sensitive indicators of the early ischemic changes that follow coronary occlusion, and may be used to assess the effects of therapeutic interventions on events resulting from a myocardial perfusion deficit.
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PMID:Study of electrophysiological ischemic events during coronary angioplasty. 1522 91