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Biomedical subjects

Wilmer W Nichols

Publications and source records attributed to Wilmer W Nichols.

At least 19 recordsLinked to original sources

Enhanced external counterpulsation treatment improves arterial wall properties and wave reflection characteristics in patients with refractory angina.

OBJECTIVES: To determine if arterial properties and wave reflection characteristics are favorably altered after enhanced external counterpulsation (EECP) treatment in patients with refractory angina. BACKGROUND: Early return of reflected waves from the lower body, resulting from increased arterial stiffness, augments central aortic pressure and increases left ventricular (LV) afterload and myocardial oxygen demand. EECP acutely enhances coronary perfusion (supply) and reduces LV afterload (demand). However, the mechanisms responsible for the sustained beneficial effects of EECP treatment are unclear. METHODS: Radial artery pressure waveforms were recorded by applanation tonometry and central aortic pressure waveforms generated using a mathematical transfer function in 20 patients with stable refractory angina. Data were collected before and after 34 1-h EECP sessions. Augmentation index (AI(a)) and timing of the reflected pressure wave were calculated from the aortic waveform. RESULTS: EECP treatment caused a decline in AI(a) and an increase in reflected wave travel time. These modifications in wave reflection characteristics caused a decrease in aortic systolic pressure and wasted LV pressure energy. The average number of angina episodes and Canadian Cardiovascular Society (CCS) class, both decreased in concordance with the physiologic changes due to EECP treatment. CONCLUSIONS: EECP treatment reduces arterial stiffness and improves wave reflection characteristics in patients with refractory angina. These changes decrease LV afterload and myocardial oxygen demand and reduce the number of angina episodes, therefore enabling patients to participate in continuous exercise programs which in turn may provide long-term benefits and sustained improved quality of life.

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Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms.

Aortic pulse wave velocity (PWV) and augmentation index are independent predictors of adverse cardiovascular events, including mortality. In hypertension and aging, central elastic arteries become stiffer, diastolic pressure decreases, and central systolic and pulse pressures are augmented due to increased PWV and early return of reflected waves to the heart from the periphery. Valuable information on arterial properties such as stiffness can be obtained from both central (aortic) and peripheral (radial artery) pressure waveforms, but absolute values of wave reflection amplitude and wasted left ventricular (LV) pressure energy can only be obtained from the central arterial pressure waveform. As the arterial system becomes stiffer, there is a marked increase in central systolic and pulse pressures and wasted LV energy, along with a decrease in pulse pressure amplification. The increase in aortic systolic and pulse pressures are due primarily to increases in PWV and wave reflection amplitude with a small increase in incident wave amplitude. In individuals with very stiff elastic arteries (eg, in older persons with isolated systolic hypertension), there is a decrease in diastolic pressure. These changes in pressure components increase LV afterload and myocardial oxygen demand and therefore cause an undesirable mismatch between ventricle emptying and arterial pulse wave transmission, which promotes ventricular hypertrophy. High systolic and pulse pressures resulting from advanced age or hypertension increase circumferential arterial wall stress, which likely causes breakdown of medial elastin and increases the possibility of local fatigue, endothelial damage and development of atherosclerosis. Vasodilator drugs may have little direct effect on large central elastic arteries, but at the same time, their effects on peripheral muscular arteries reduce wave reflection amplitude and markedly lower systolic and pulse pressures and ventricular afterload. These beneficial effects on central arterial pressure can occur with or without a reduction in cuff blood pressure (BP) and may explain the apparent "pressure-independent" effects of drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Therefore, optimal treatment of high BP and its complications should include consideration of arterial stiffness, augmentation of aortic pressure, and LV wasted energy, all of which should be reduced to the lowest possible level.

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Effect of exercise training on endothelial function in men with coronary artery disease.

The objective of this study was to investigate the effects of 12 weeks of standard cardiac rehabilitation on endothelial function, oxidative stress, and antioxidant defenses in patients with coronary artery disease. Twelve weeks of endurance exercise training led to an improvement in endothelial function as measured by brachial artery flow-mediated dilation (7.9% at baseline vs 11.1% at 12 weeks). Exercise training resulted in increased plasma nitrite and nitrate levels, increased plasma superoxide dismutase activity, and decreased oxidative stress.

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Effect of exercise training on central aortic pressure wave reflection in coronary artery disease.

BACKGROUND: Arterial stiffness is an important factor for cardiovascular performance and a predictor of cardiovascular risk. We investigated the effect of exercise training on arterial stiffness in coronary artery disease (CAD). METHODS: Arterial stiffness was assessed before and after 12 weeks of either exercise training or standard care in CAD patients. Arterial stiffness was evaluated by aortic augmentation index and time delay of the reflected wave (Deltat) using the SphygmoCor system. RESULTS: The augmentation index decreased (30% v 26%, P <.05) and Deltat increased (136 msec v 144 msec, P <.05) in patients with CAD after 12 weeks of exercise. CONCLUSION: These results suggest that endurance exercise training improves systemic arterial stiffness in individuals with CAD.

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Radial artery tonometry demonstrates arterial stiffness in children with type 1 diabetes.

OBJECTIVE: To determine if children with type 1 diabetes have increased arterial stiffness by estimating augmentation index with the simple noninvasive technique of radial artery tonometry. RESEARCH DESIGN AND METHODS: We studied 98 type 1 diabetic children and 57 healthy control subjects, ages 10-18 years, matched for age, sex, race, and BMI, generating 43 matched pairs. Radial artery tonometry was performed, and blood was collected for analysis of fasting lipids, HbA1c, glucose, and cytokines in all children. RESULTS: Children with diabetes had a significantly higher augmentation index corrected to a heart rate of 75 (AI75) than their matched control subjects. Mean AI75 in type 1 diabetic subjects was 1.11 +/- 10.15 versus -3.32 +/- 10.36 in control subjects. The case-control difference was 5.20 +/- 11.02 (P=0.0031). CONCLUSIONS: Children with type 1 diabetes have increased arterial stiffness compared with healthy control subjects. Radial artery tonometry is a simple noninvasive technique that could be added to the armamentarium of tests used to provide cardiovascular risk stratification in children with type 1 diabetes.

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Vascular effects of sildenafil in hypertensive cardiac transplant recipients.

BACKGROUND: Sildenafil is commonly used in the treatment of erectile dysfunction in hypertensive male cardiac transplant recipients (CTR); however, little is known about the vascular effects of sildenafil in these patients. METHODS: Central and peripheral arterial blood pressure (BP), heart rate, and brachial artery reactivity were determined in 15 hypertensive male CTR before and after oral sildenafil (50 mg) administration. RESULTS: Sildenafil improved brachial and aortic systolic BP, pulse pressure, aortic augmentation index, left ventricular tension time index, travel time of the reflected aortic pressure wave, and brachial artery reactivity (P <.01 for each comparison). No patient became hypotensive with sildenafil despite continuation of usual antihypertensive medications. CONCLUSIONS: Sildenafil (50 mg) is well tolerated in hypertensive CTR and improves BP, aortic augmentation index, and endothelial function. By decreasing the amplitude of the reflected pressure wave and delaying its return to the heart, sildenafil reduces left ventricular afterload and systolic stress.

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