Tetsu Yamakado

The relationship between aortic augmentation index and pulse wave velocity: an invasive study.

Objectives The aortic augmentation index (AI) and aortic pulse wave velocity (PWV) are known to be indicators of arterial stiffness. However, it is not clear whether aortic AI and PWV reflect aortic stiffness in similar ways. We investigated the relationship between aortic AI and PWV by measuring them directly using a catheter technique. Design and methods Forty-one patients, aged 34–79 years, were studied during diagnostic cardiac catheterization. Aortic pressures were measured using a catheter-tip manometer at two points, one in the ascending aorta and one 40 cm distally in the descending aorta. Aortic AI was defined as the difference between early and late pressure peaks divided by the pulse pressure of the ascending aorta. Aortic PWV was calculated as the distance between the two measuring sites divided by the transit time. We also examined the effects of vasodilatation on AI and PWV by the intra-aortic administration of nitroglycerin in 15 patients. Results AI was significantly related to age, systolic aortic pressure, heart rate, left ventricular ejection time, and height. Aortic PWV showed an association only with age and systolic aortic pressure. There was no significant relationship between aortic AI and PWV (r = 0.28, NS). Nitroglycerin also produced different effects on aortic AI and PWV: aortic AI was significantly decreased (−0.17, P < 0.01) after nitroglycerin, but PWV remained unchanged (+0.4 m/s, NS). Conclusions Aortic AI and PWV cannot be used interchangeably as an index of arterial stiffness. AI may not be a true indicator of arterial stiffness, but an index of wave reflection including PWV.

Exercise-induced coronary spasm: comparison of treadmill and bicycle exercise in patients with vasospastic angina.

Background We investigated whether exercise-induced coronary spasms are influenced by the different exercise modes.Methods We compared ischaemic ECG responses in 67 patients with vasospastic angina who underwent both treadmill and bicycle ergometer exercise and also coronary angiography.Results ECG ST-segment elevation was provoked more frequently during treadmill exercise than it was during bicycle exercise (19 versus 9%, P<0.05). Of 45 patients without significant coronary stenosis (coronary artery luminal diameter narrowing < 75%), 19 patients manifested ST-segment depression during treadmill exercise, whereas only seven patients did during bicycle exercise (42 versus 16%, P<0.01). All patients with ST-segment elevation or depression during bicycle ergometer exercise also had ST-segment changes during treadmill exercise. Although higher systemic blood pressure levels and lower heart rates were found during bicycle exercise compared with during treadmill exercise, the pressure-rate products at peak exercise did not differ between the two exercise tests.Conclusions It seems that treadmill and bicycle exercise are different stressors in patients with vasospastic angina, and that coronary spasms are provoked more frequently during treadmill exercise than they are during bicycle exercise. The cause of this difference is not known, but it may be related in part to the difference in systemic haemodynamic or neurohumoral response.

Left ventricular inotropic and lusitropic responses to pacing-induced tachycardia in patients with varying degrees of ventricular dysfunction

BACKGROUND In the failing human heart contractile reserve during tachycardia is attenuated or absent. However, it is not known whether during tachycardia diminished inotropic reserve depends on the degree of ventricular dysfunction or lusitropic reserve is also diminished in patients with left ventricular (LV) dysfunction. METHODS We studied 18 patients with dilated cardiomyopathy or mildly depressed LV function and 13 subjects in a control group (ejection fraction 0.67+/-0.09). The patients were classified into two groups based on whether their ejection fraction was less than or more than 0.40 (group 1, ejection fraction 0.27+/-0.05; group 2, ejection fraction 0.49+/-0.07). LV pressures were measured with a catheter-tip manometer during incremental right atrial pacing up to a heart rate of 150 beats/min. RESULTS With incremental pacing LV peak positive dP/dt rose progressively in both the normal group and in group 2, but the increase was less for group 2 than for the normal group; in group 1 the increase was slight or absent. In contrast, a significant and progressive decrease occurred in the time constant of LV relaxation in all three groups. Although their values remained significantly different at each heart rate, no intergroup differences in absolute or percent changes were present. CONCLUSIONS These findings suggest that during tachycardia LV inotropic reserve may be diminished depending on the degree of ventricular dysfunction, and lusitropic reserve may be preserved in patients with depressed function despite an attenuated inotropic response.

Pacing tachycardia exaggerates left ventricular diastolic dysfunction but not systolic function and regional asynergy or asynchrony in patients with hypertrophic cardiomyopathy.

AIMS Myocardial ischaemia and angina have been demonstrated in patients with hypertrophic cardiomyopathy (HCM). We hypothesized that left ventricular (LV) systolic or diastolic dysfunction would be provocated by pacing tachycardia in patients with HCM. METHODS AND RESULTS We investigated LV global and regional systolic and diastolic function in 17 patients with HCM without LV outflow obstruction and 7 normal subjects by analysing LV angiograms and simultaneously obtained high-fidelity LV pressures before and after rapid cardiac pacing (150 b.p.m.). Biplane LV silhouettes were digitized frame by frame (50 frames/s). To quantify regional dynamics, the ventricular area of the right anterior oblique projection was divided into six sections originating from the midpoint of the long axis at end-diastole. There were no significant changes in LV function after pacing in normal subjects. In HCM, the ejection fractions remained unchanged. However, LV end-diastolic pressures rose (+12 mmHg, P < 0.01), and the time constants of isovolumic pressure decay were significantly increased (T(1/2): +5.2 ms, P < 0.01; T(1/)(e): +6.8 ms, P < 0.01). The LV global diastolic pressure-volume relationships and regional diastolic pressure-area relationships of regional myocardium shifted upward (indicating decreased diastolic distensibility) in all patients. These diastolic abnormalities were not accompanied by regional asynchrony or asynergy. CONCLUSION Most patients with HCM have a reduced reactive capacity to chronotropic stress, which is haemodynamically characterized by evenly distributed diastolic dysfunction. In contrast with coronary artery disease, these diastolic abnormalities were not accompanied by systolic dysfunction, regional asynchrony, asynergy, or inhomogenous diastolic distensibility.