Naomitsu Kuji

Prediction of Optimal Atrioventricular Delay in Patients with Implanted DDD Pacemakers

In patients with an implanted DDD pacemaker (PM), the atrial contribution may be interrupted by too short an atrioventricular (AV) delay, and filling time may be shortened by too long an AV delay. The AV delay at which the end of the A wave on transmitral flow coincides with complete closure of the mitral valve may be optimal. The subjects were 15 patients [70.3 ± 12.3 (SD) years old] with an implanted DDD PM. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan‐Ganz catheter. Transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 msc. When the AV delay was set at 155 ± 26 ms, the end of the A wave coincided with complete closure of the mitral valve. When the AV delay was prolonged 25, 50, 75, and 100 ms from this AV delay, the interval between the end of the A wave and complete closure of mitral the valve was prolonged 16 ± 5, 39 ± 6, 65 ± 4 and 88 ± 5 ms, respectively (r = 0.97, P < 0.0001) and diastolic mitral regurgitation was observed during this period. Thus, the optimal AV delay may be predicted as follows: the slightly prolonged AV delay minus the interval between the end of the A wave and complete closure of the mitral valve. When the AV delay was set at 215 ms, there was a significant positive correlation between the predicted optimal AV delay (166 ± 23 ms) and the optimal AV delay (CO: 161 ± 26 msec, r = 0.93, P < 0.0001. PCWP: 161 ± 28 msec, r = 0.95, P < 0.0001). In conclusion, optimal AV delay can be predicted by this simple formula: slightly prolonged AV delay minus the interval between end of A wave and complete closure of mitral valve at the AV delay setting.

Critical PQ Interval for the Appearance of Diastolic Mitral Regurgitation and Optimal PQ Interval in Patients Implanted with DDD Pacemakers

Diastolic mitral regurgitation (MR) may be induced by prolonging atrioventricular (AV) delay, and a significant negative correhtion has been described between tbe critical PQ interval for the appearance of diastolic MR and pulmonary capillary wedge pressure (PCWP) in patients with DDD pacemakers. We report the relationship between the critical PQ interval for the appearance of diastolic MR and the optimal PQ interval in 11 patients (69.1 ± 12.6 years). Cardiac output (CO) and PCWP were measured by Swan‐Ganz catheter and transmitral blood flow was recorded by pulsed‐Doppler echocardiography. AV delay was prolonged stepwise by 0.025 seconds starting from 0.065 seconds. The pacing rate was fixed at 70 beats/min. CO was highest when the PQ interval was 0.18 ± 0.04 seconds. There was a significant positive correlation between the critical PQ interval for the appearance of diastolic MR and the PQ interval at which CO was the highest (r = 0.91, P < 0.01). The PQ interval at which CO was the highest was 0.02 ± 0.02 seconds shorter than the critical PQ interval for the appearance of diastolic MR (P < 0.05). When the PQ interval was increased by 0.025 seconds from the critical PQ interval for the appearance of diastolic MR, CO decreased from 4.3 ± 0.6 L/min to 4.1 ± 0.6 L/min and PCWP increased from 7.5 ± 6.4 mmHg to 8.5 ± 7.3 mmHg (P < 0.05). In conclusion, the critical PQ interval for the appearance of diastolic MR may represent the upper limit of the optimal PQ interval and the AV delay should be set to not exceed the critical PQ interval for the appearance of diastolic MR.

Value of ST-segment elevation pattern in predicting infarct size and left ventricular function at discharge in patients with reperfused acute anterior myocardial infarction

BACKGROUND The implication of the shape of ST elevation in the acute phase of myocardial infarction (MI) remains unclear. METHODS AND RESULTS We examined the relation between the shape of ST elevation and infarct size in 77 patients who had a first acute anterior MI with successful reperfusion within 6 hours from symptom onset. A 12-lead electrocardiogram was recorded immediately before reperfusion confirmed by coronary angiography. The shape of ST elevation in lead V3 was classified into 3 types: concave type (n = 24), straight type (n = 41), and convex type (n = 12). For concave type, straight type, and convex type, a median value of peak creatine kinase was 2287, 4371, and 5322 mU/mL, and left ventricular ejection fraction measured by left ventriculography at discharge (14 days after MI) was 58%, 48%, and 41% (P <.05; concave type versus the other 2 types), respectively. A multivariate logistic regression model demonstrated that the concave type of ST elevation was a strong predicting factor for preserved left ventricular function (left ventricular ejection fraction >/=50% at discharge; odds ratio 6.2, 95% confidence interval 1.6 to 20.8, P =.019). CONCLUSIONS In patients with reperfused acute anterior MI, left ventricular function was excellent in patients with concave type, intermediate in those with straight type, and relatively poor in those with convex type ST elevation at discharge. This simple classification is useful for predicting left ventricular function at discharge.

Angiotensin II attenuates the vasodilating effect of a nitric oxide donor, glyceryl trinitrate: Roles of superoxide and angiotensin II type 1 receptors

The development of tolerance to organic nitrates limits their usefulness in the treatment of heart disease. Activation of the renin‐angiotensin system by heart failure itself and by nitrate therapy may be one possible mechanism underlying nitrate tolerance. We investigated the effect of subpressor doses of angiotensin II on the vasodilating effect of glyceryl trinitrate in human forearm resistance vessels of healthy male subjects by using venous occlusion strain‐gauge plethysmography.

Relation of absence of ST reelevation immediately after reperfusion and success of reperfusion with myocardial salvage

To examine whether resolution in ST elevation without ST reelevation immediately after reperfusion indicates successful reperfusion with myocardial salvage, we studied 40 patients who had an extensive acute myocardial infarction with early reperfusion: 24 patients had ST reelevation and 16 patients had no ST reelevation. Results indicate that (1) in the group with ST reelevation, rapid progression of myocardial damage occurs by reperfusion itself (i.e., reperfusion injury) and (2) in the group without ST reelevation, myocardial damage had already been extensive and irreversible at the time of reperfusion; thus, the absence of ST reelevation is not always a sign of reperfusion with myocardial salvage.

Angiotensin II Attenuates Vasodilatation Induced by No-Donor, Glyceryl Trinitrate: Role of Super Oxide and Angiotensin Type 1 Receptor

P25 We investigated effects of subpressor dose of angiotensin II (ANG II) on the vasodilating effect of Glyceryl trinitrate (GTN)in 9 normotensive healthy males. GTN at 100, 250, 1000 ng/min was intra-arterially infused with ANG II at 1, 5 pmol/min or placebo (protocol 1) with noradrenaline (NA) at 50 pmol/min or placebo (protocol 2). Effect of intra-arterial infusion of vitamin C at 25 mg/min on the interaction between GTN and ANG II was also tested (protocol 3).Protocol 1 was repeated after single oral dose of angiotensin type 1 receptor blocker, Candesartan (8mg) or matched placebo (protocol 4). Forearm blood flow (FBF) was measured by strain gauge plethymograph. ANG II significantly and dose-dependently attenuated the vasodilating effect of GTN (means±S.D. of % changes of FBF: 28±8, 79±22, 208±28 % at 100, 250, 1000 pmol/min of GTN with placebo, 8±6, 47±13, 173±31 with ANG II 1 pmol/min, 2±10, 39±13, 132±23 with ANG II 5 pmol/min. P=0.0057 vs placebo by ANOVA).NA did not affect the vasodilating effect of GTN. Co-infusion of vitamin C (25 mg/min)completely abolished the the interaction between ANG II and GTN. Attenuation of the effect of GTN by ANG II disappeared after the single dose of Candesartan. In summary, subpressor dose of ANG II attenuated the effect of GTN. There was a lack of effect of ANG II in the presence of either vitamin C or Candesartan. Our results suggest that ANG II may stimulate superoxide production through AT1 receptor which inactivates NO by forming peroxynitrite.