Using an isolated perfused rat heart preparation, the protective effects of lidocaine and diltiazem on ischemic derangements of myocardial energy metabolism were studied with 31P-nuclear magnetic resonance spectroscopy. The hearts were perfused with a solution containing lidocaine (4.27×10-5, 12.80×10-5M) or diltiazem (2.22×10-7, 2.22×10-6M) for 15min prior to the induction of global ischemia. The decrease in myocardial oxygen consumption rate, assessed as the product of heart rate and left ventricular systolic pressure (HR×LVP), was greater in diltiazem-treated than in lidocaine-treated hearts. Diltiazem and lidocaine significantly retarded the fall in myocardial pH during ischemia and improved ATP recovery after reperfusion. There was a good correlation between suppression of HR×LVP observed before induction of ischemia and decreased drop in pH during the early phase of ischemia in the diltiazem-treated groups (r=-0.78, p<0.01), but not in the lidocaine-treated groups. These results indicate that the beneficial effects of diltiazem on the ischemic myocardium are due primarily to the cardiodepressant effects. The beneficial effects of lidocaine cannot, however, be explained solely on the basis of the depression of oxygen consumption.
Analysis of beat to beat changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in 30 consecutive patients undergoing diagnostic cardiac catheterization. The group consisted of 9 normal subjects, 18 with coronary artery disease and 3 with congestive cardiomyopathy. The recordings of aortic pressure were made during atrial pacing and ventricular pacing at a rate 5 to 10 beats/min above each individual's sinus rhythm. During ventricular pacing, LV ejection time was the longest when an atrial contraction preceded a ventricularly paced beat by a physiologic interval and was approximately similar to that obtained during atrial pacing (maxET). When the atrial systole occurred with or followed the ventricularly paced contraction, LV ejection time was decreased (minET). Since maxET occurred in the presence of an effective atrial contraction to ventricular filling and minET in the absence of this contraction, the atrial contribution to ventricular filling was calculated as (maxET-minET)/maxET X 100 (%). LV volumes at end-systole (V1), before atrial contraction (V2) and at end-diastole (V3) were obtained according to the area-length method by tracing the silhouette of left ventriculograms using a computer system. The atrial contribution was calculated from LV volumes using the formula (V3-V2)/(V3-V1) X 100 (%). There was a good correlation (r = 0.88) between the atrial contributions calculated from LV ejection times and those calculated from LV volumes. In the patients with coronary artery disease and with congestive cardiomyopathy, the atrial contribution was significantly greater than in the normal subjects. The measurement of LV ejection time during ventricular pacing may be a clinically useful screening procedure to identify patients in whom physiologic pacing may be indicated.
A female patient with severe aortic stenosis had suffered from repeated syncope. Transaortic valve pressure gradient at cardiac catheterization was 117 mmHg. Continuous electrocardiographic monitoring was done after admission. During syncope, the electrocardiogram showed bradycardia with the lowest heart rate 44 beats per minute, while arterial pulses were not palpable. Rather than arrhythmia, other mechanisms, such as an inhibitory reflex from left ventricular receptors, should be postulated as the cause of syncope in patients with severe aortic stenosis.
BACKGROUND Improvement of exertional dyspnea occurs immediately after percutaneous transvenous mitral commissurotomy (PTMC), but the pathophysiological basis for this early symptomatic improvement has not been elucidated. METHODS AND RESULTS Exercise hemodynamic measurement and exercise ventilatory measurement with arterial blood gas analysis were performed in 21 patients aged 50.4 +/- 9.5 years (mean +/- SD) with symptomatic mitral stenosis before and a few days after PTMC. Exercise ventilatory measurement were also performed in 14 normal control subjects aged 48.9 +/- 4.9 years. After PTMC, mitral valve area increased (from 1.0 +/- 0.3 to 1.7 +/- 0.3 cm2, P < .001), mean mitral gradient (from 12.2 +/- 5.2 to 5.2 +/- 2.2 mm Hg, P < .001), and mean left atrial pressure (from 18.7 +/- 6.1 to 12.1 +/- 4.0 mm Hg, P < .001) decreased. All patients experienced significant symptomatic improvement soon after PTMC. Comparison of hemodynamic parameters at the same ergometer work rate showed a significant decrease in pulmonary artery systolic pressure (from 77 +/- 18 to 67 +/- 14 mm Hg, P < .001) and diastolic pressure (from 36 +/- 10 to 28 +/- 7 mm Hg, P < .001) and a significant increase in cardiac output (from 6.4 +/- 1.4 to 8.1 +/- 1.9 L/min, P < .001). Despite the improvement in exercise hemodynamics and symptoms, exercise capacity determined by peak oxygen uptake (from 18.0 +/- 2.9 to 18.6 +/- 3.1 mL.kg-1 x min-1) and anaerobic threshold (from 11.7 +/- 2.4 to 12.0 +/- 2.4 mL.kg-1 x min-1) remained unchanged. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output, decreased significantly from 37.2 +/- 6.7 to 33.9 +/- 5.8 (P < .001), but remained significantly higher than that in the normal subjects (27.9 +/- 3.6, P < .01). The ratio of total dead space to tidal volume and total dead space per breath during exercise decreased significantly after PTMC (P < .05). The change in excessive exercise ventilation after PTMC was correlated with the change in dead space to tidal volume ratio (r = .59). CONCLUSIONS Significant relief of exertional dyspnea immediately after PTMC is not accompanied by an improvement in exercise capacity. A decrease in excessive ventilation due to a decrease in physiological dead space resulting from hemodynamic improvement partly contributes to the early relief of symptoms after PTMC. However, lung compliance, which was not measured in the present study, may have changed after PTMC. This change may also contribute to the symptomatic improvement.
The aim of this study was to investigate the role of nitric oxide (NO) in the coronary circulation and its relation to basal coronary artery tone in patients with vasospastic angina (VSA). We evaluated the level of nitric oxide end-products (NOx; nitrite + nitrate) in coronary circulation blood using an HPLC-Griess system for nine patients with VSA and nine control patients. All of the patients with VSA experienced focal spasm in the proximal to middle segments of the left anterior descending coronary artery (LAD) in response to intracoronary injection of ergonovine maleate. The luminal diameter of the coronary artery was measured in each patient by quantitative coronary arteriography. Blood samples for NOx measurement were obtained from the coronary sinus (NOxV) and the ostium of the left coronary artery (NOxA). The NOx difference, calculated from the coronary venous-arterial difference in NOx, was close to zero for the control patients whereas it was clearly negative for the patients with VSA. In addition, the NOx difference in the patients with VSA showed a negative correlation with basal coronary artery tone (r = - 0.91, p < 0.01) and a positive correlation with the dose of ergonovine required for spasm provocation (r = 0.77, p < 0.05). These results indicate that increased basal coronary artery tone and higher susceptibility to ergonovine in patients with VSA would be a consequence of coronary endothelial dysfunction as is indicated by NOx.
The optimal amplitude and slew rate of intracardiac electrograms for pacemaker sensing were examined on a theoretical basis by computer simulation. The simulation was based on the concept that it is the voltage at the position of the pacing electrode in an electrical field of a moving electrical dipole. By changing the distance between the electrode and the myocardium and the moving velocity of the electrical dipole, simulated ECGs with arbitrary amplitudes and slew rates were generated by the computer and fed to a bandpass filter. This filter was equivalent to those assembled in some models of permanent pacemakers and had a center pass-band frequency of 50 Hz and a Q of 1.0. The outputs of the filter were measured. The results showed that, for pacemakers sensing, simulated intracardiac electrograms with high amplitude should have high slew rates and those with low amplitudes should have low slew rates, although the absolute values depend on the characteristics of the bandpass filter and the sensing threshold of the pacemaker.
The implantable defibrillator, developed by Dr Michel Mirowski, is a remarkable electric therapeutic device which has been in clinical use since 1980 in the treatment of life-threatening arrhythmia. However, as the present life span of this device is only 3 years, research is being carried on to extend the lifetime with improved stimulation methods, circuits and electrodes. In particular, the electrode system which is inserted into the right ventricle has more than 50 times the electrode area of a pacing electrode and is prone to degradation. What is needed is biocompatibility and electrical stability, similar to that of cardiac pacemaker electrodes, which can be used for more than 10 years. For this purpose, we focused on a conductive ceramic as a new material for the defibrillation electrode instead of the previously-used metal. We selected glassy carbon as our electrode material and tested the surface condition through acute and chronic animal experiments. No clots formed around the electrodes after a 3-month implantation, nor were there surface disorders after the defibrillation stimulations. We concluded that glassy carbon is a promising material for future defibrillation electrodes.
