MRI measurements of coronary flow and flow reserve were in good agreement with US measurements. In addition, MRI measurements of coronary flow reserve successfully discriminated stenotic from normal vessels. These results indicate that MRI is a useful method for the noninvasive assessment of coronary flow and stenosis.

Phase-contrast magnetic resonance imaging (PC-MRI) can be used to produce multiframe cine flow images of the coronary arteries. Accurate coronary flow measurement requires the elimination of respiratory motion artifacts using k-space segmentation to acquire the data in a single breath-hold. However, the duration of the breath-hold is proportional to the number of cine frames. In the present study, the number of cine frames was varied and the accuracies of the coronary flow measurements were assessed using perivascular US. For the range of flows studied (2 ml/min to 147 ml/min), the correlation coefficients for PC-MRI and US increased (.70-.98) and the limits of agreement improved (+/-45 ml.min-1 to +/-10 ml.min-1) as the number of cine frames increased from one to six. The results suggest that the accuracy of breath-hold cine PC-MRI measurements of coronary artery flow improves as the number of cine frames increases.

Prolonged depression of segmental systolic thickening after brief coronary artery occlusion may result principally from events during reperfusion rather than during the ischemic interval. Thus, cellular calcium overload at reperfusion may be a mediator of contractile dysfunction after brief ischemia, and reduction of calcium entry by diltiazem, a calcium channel antagonist, may enhance recovery of systolic thickening after brief periods of ischemia. Thirteen awake unsedated dogs instrumented with hemodynamic catheters, left anterior descending coronary artery occluders and five to six pairs of intramyocardial sonomicrometers underwent two 15 min coronary artery occlusions with 24 h reperfusion. The order of infusion of diltiazem (15 micrograms/kg per min) or saline solution was alternated. Systolic thickening, hemodynamic variables and regional myocardial blood flow were measured serially over 24 h. Despite equally severe ischemic dysfunction during coronary occlusion, diltiazem-treated segments with systolic thinning during ischemia recovered control segmental thickening significantly earlier than saline solution-treated segments (at 30 versus 180 min of reperfusion). Blood pressure was mildly decreased during diltiazem treatment; therefore, a second group of 10 dogs underwent a similar occlusion and reflow period during infusion of nitroprusside to lower mean arterial pressure equivalently. Decreases in blood pressure in this group resulted in some improvement in segmental systolic function; however, this did not reach statistical significance at any time. Regional myocardial blood flows were similar in the saline solution- and diltiazem-treated groups during ischemia and reflow. Thus, it is concluded that 1) diltiazem infusion significantly enhanced recovery of segmental systolic thickening after 15 min of ischemia and 24 h of reperfusion; 2) the enhancement in segmental systolic function could not entirely be attributed to decreased mean arterial pressure; 3) improvement in postischemic segmental ventricular function was seen only in those segments with systolic thinning during ischemia; thus, segments with the most severe ischemic dysfunction benefited most; and 4) there were no important differences in regional myocardial blood flow during ischemia and reperfusion between saline- and diltiazem-treated animals.

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.

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We investigated entrainment in a pacemaker model of reentrant ventricular tachycardia (VT) created in the intact dog heart using a VAT pacemaker with both electrodes on the ventricular epicardium. This produced an incessant wide QRS tachycardia originating from the pacing site with a cycle length equal to the conduction time between the sensing and pacing site plus the pacemaker AV delay. The conduction time between entrainment sites and the critical elements of the reentrant pathway (sensing and pacing sites) was determined by pacing at a comparable cycle length during sinus rhythm. Entrainment was achieved in 12 tachycardias with pacing at 1-4 sites at cycle lengths 10-100 msec shorter than tachycardia and confirmed by constant QRS fusion, progressive QRS fusion, and coupling of the first nonpaced QRS or intracardiac electrogram at the entraining cycle length. By least squares regression, the timing of entrainment onset (first reset of pacing or sensing site electrogram) measured by the prematurity of the local electrogram at the entraining site was highly correlated to the shortest conduction time between the entraining site and the circuit (F value of 84.7 and R = 0.752 [P less than 0.001]). Therefore, the timing of entrainment onset maybe useful in predicting the conduction time from the entraining site to critical elements of a reentrant circuit and may assist in localization of the reentrant pathway.

Although left ventricular hypertrophy with hypertension did not attenuate the contractile response to reperfusion, hypertrophy with reduced blood pressure was associated with significantly greater depression of segmental systolic thickening early during reperfusion.

No abstract