Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effects of coronary artery occlusion and pacing from ventricular sites on the relation of the maximum rate of rise of left ventricular pressure (dP/dtmax) to the end-diastolic volume (VED) in dogs previously instrumented to measure left ventricular pressure and to determine left ventricular volume from three ultrasonically measured dimensions. The dP/dtmax-VED relation was generated by vena caval occlusion and compared with the simultaneously produced end-systolic pressure-end-systolic volume (PES-VES) relation. The dP/dtmax-VED relation was described by a straight line during all conditions. Occlusion of the left circumflex coronary artery produced a rightward shift of the dP/dtmax-VED relation, increasing the volume intercept by 11.3 +/- 5.3 (SD) ml (P less than 0.05). Compared with atrial pacing, the dP/dtmax-VED relation was shifted to the right with the volume intercept increasing by 4.8 +/- 4.4 ml (P less than 0.05) during pacing from the right ventricular free wall, 3.7 +/- 5.0 ml (P less than 0.05) during pacing from the right ventricular apex, and 3.7 +/- 2.4 ml (P less than 0.05) during pacing from the left ventricular free wall. Similar increases were observed in the volume intercepts of the PES-VES relations during coronary occlusion or ventricular pacing. These results are consistent with the predictions of the time-varying elastance model and support its use as a conceptual framework to understand left ventricular performance during isovolumic contraction and at end systole, both in the normal ventricle and the ventricle with regional abnormalities of contraction.
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PMID:Effects of regional ischemia and ventricular pacing on LV dP/dtmax-end-diastolic volume relation. 357 43

Calcium channel antagonists can reduce calcium overload induced by myocardial ischemia and thereby protect against malignant arrhythmias. However, these drugs may also adversely affect cardiac contractile function. Mibefradil is a new calcium antagonist that can inhibit cardiac calcium current without reducing myocardial force development. The effects of mibefradil on the inducibility of arrhythmias both before and during ischemia were therefore evaluated in animals with healed infarctions. First, a 2-min coronary occlusion was made during the last minute of exercise (n = 48): 25 animals had ventricular fibrillation (susceptible), whereas 23 did not (resistant). On a subsequent day, programmed electrical stimulation (PES, 8 paced beats followed by two extrastimuli) induced ventricular tachycardia in 19 of 25 susceptible animals but in none of the resistant animals (chi square = 24.6, P < .001). Verapamil (n = 14), diltiazem (n = 13) and mibefradil (n = 14) elicited significant dose-dependent decreases in refractory period and in the Q-Tc interval (except mibefradil) yet failed to prevent PES-induced arrhythmias. Diltiazem and verapamil also increased P-R interval and reduced the maximum rate of change of left ventricular pressure, whereas mibefradil did not. However, all three drugs abolished arrhythmias induced by PES during ischemia. In contrast, lidocaine suppressed PES-induced arrhythmias but failed to prevent ischemically induced arrhythmias. Thus mibefradil can prevent ischemically induced ventricular fibrillation without adverse actions on either A-V nodal conduction or contractile function. These data further suggest that calcium entry may play a critical role in the initiation of ventricular fibrillation during ischemia, whereas other factors must be responsible for the extrasystoles induced by PES.
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PMID:The effects of mibefradil, a novel calcium channel antagonist on ventricular arrhythmias induced by myocardial ischemia and programmed electrical stimulation. 866 18