Exercise Physiology in the Cath Lab: Still Alive and Well!
ABSTRACT Writing on the topic of 'pectoris dolor': "With respect to the treatment of this complaint, I have little or nothing to advance: nor indeed is it to be expected we should have made much progress in the cure of a disease, which has hitherto hardly had a place, or a name in medical books... Opium taken at bed-time will prevent the attacks at night. I know one who set himself a task of sawing wood for half an hour every day, and was nearly cured."(1) The salient observation defining the clinical syndrome of 'warm-up' angina, namely that anginal symptoms may be reduced with repeated episodes of work, was initially made over 200 years ago by the London physician William Heberden. Consistent with his original description, contemporary demonstrations of warm-up angina either involves greater time to ischemic signs or symptoms (i.e. ST segment depression or chest pain) or a reduction in ischemic manifestations at equivalent work load in patients with coronary artery disease (CAD) undergoing repeated bouts of exercise. Multiple theories have been advanced to explain this physiologic phenomenon, ranging from changes in myocardial signaling to increased collateral recruitment and ischemic preconditioning.(2-4) Greater appreciation of physiologic adaptations occurring with exercise vis a vis ventricular vascular coupling combined with novel methodologic approaches have provided fresh mechanistic insight and advanced our understanding of this clinical entity.(5-7).
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ABSTRACT: This study investigated the effect of age and gender on central arterial hemodynamic variables derived from noninvasive tonometric carotid pressure waveforms. Women have a greater age-related increase in left ventricular (LV) mass than do men and are more likely to experience symptomatic heart failure after infarction despite their higher ejection fraction. In studies of these changes, ventricular afterload is incompletely defined by brachial blood pressure (BP) measurements. We hypothesized that there exist gender differences in pulsatile vascular load, as revealed by pressure waveform analysis, which may produce suboptimal afterload conditions in women. Data from 350 healthy normotensive subjects (187 female) aged 2 to 81 years were analyzed in decade groups. Augmentation index (AIx, the difference between early and late pressure peaks divided by pulse pressure) was used as an index of pulsatile afterload, and the ratio of diastolic to systolic pressure-time integral gave a subendocardial viability index. Heart rate, BP, ejection duration and maximal rate of pressure rise (dP/dt(max)) were also determined. Male subjects had a slightly higher systolic pressure until age 50. Female subjects had higher systolic pressure augmentation after the 1st decade, a difference that was significant after age 30 (p < 0.005 for each decade). In both males and females there was a strong age dependence for AIx (r = 0.77, p < 0.001 for females, r = 0.66, p < 0.001 for males). Although males had a larger body size and higher systolic pressure, systolic pressure-time integral was similar in males and females across all age groups. Diastolic pressure-time integral was consistently lower in females because of their shorter diastolic period. Subendocardial viability index was lower in females across the entire group. Differences in stature and heart rate may contribute to these findings. These new data may help to explain previous findings in women of an age-related increase in LV mass and excess symptomatic heart failure that are not explained by differences in brachial BP.Journal of the American College of Cardiology 01/1998; 30(7):1863-71. DOI:10.1016/S0735-1097(97)00378-1 · 15.34 Impact Factor
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ABSTRACT: Objectives: This study was designed to examine if exercise-induced ischemia initiated late preconditioning in humans that becomes manifest during subsequent exercise and serial balloon occlusion of the left anterior descending coronary artery (LAD). Background: The existence of late preconditioning in humans is controversial. We therefore compared myocardial responses to exercise-induced and intracoronary balloon inflation–induced ischemia in two groups of patients subjected to different temporal patterns of ischemia. Methods: Thirty patients with stable angina secondary to single-vessel LAD disease underwent percutaneous coronary intervention (PCI) after two separate exercise tolerance test (ETT) protocols designed to investigate isolated early preconditioning (IEP) alone or the second window of protection (SWOP). The IEP subjects underwent three sequential ETTs at least two weeks before PCI. The SWOP subjects underwent five sequential ETTs commencing 24 h before PCI. Results: During PCI there was no significant difference in intracoronary pressure–derived collateral flow index (CFI) between groups (IEP = 0.15 ± 0.13, SWOP = 0.19 ± 0.15). In SWOP patients, compared with the initial ETT, the ETT performed 24 h later had a 40% (p < 0.001) increase in time to 0.1-mV ST depression and a 60% (p < 0.05) decrease in ventricular ectopic frequency. During the first balloon inflation, peak ST elevation was reduced by 49% (p < 0.05) in the SWOP versus the IEP group, and the dependence on CFI observed in the IEP group was abolished (analysis of covariance, p < 0.05). The significant attenuation of ST elevation (47%, p < 0.005) seen at the time of the second inflation in the IEP patients was not seen in the SWOP patients. Conclusions: Exercise-induced ischemia triggers late preconditioning in humans, which becomes manifest during exercise and PCI. This is the first evidence that ischemia induced by coronary occlusion is attenuated in humans by a late preconditioning effect induced by exercise.Journal of the American College of Cardiology 04/2003; 41(7). DOI:10.1016/S0735-1097(03)00055-X · 15.34 Impact Factor
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ABSTRACT: Exercise markedly influences pulse wave morphology, but the mechanism is unknown. We investigated whether effects of exercise on the arterial pulse result from alterations in stroke volume or pulse wave velocity (PWV)/large artery stiffness or reduction of pressure wave reflection. Healthy subjects (n = 25) performed bicycle ergometry. with workload increasing from 25 to 150 W for 12 min. Digital arterial pressure waveforms were recorded using a servo-controlled finger cuff. Radial arterial pressure waveforms and carotid-femoral PWV were determined by applanation tonometry. Stroke volume was measured by echocardiography, and brachial and femoral artery blood flows and diameters were measured by ultrasound. Digital waveforms were recorded continuously. Other measurements were made before and after exercise. Exercise markedly reduced late systolic and diastolic augmentation of the peripheral pressure pulse. At 15 min into recovery, stroke volume and PWV were similar to baseline values, but changes in pulse wave morphology persisted. Late systolic augmentation index (radial pulse) was reduced from 54 +/- 3.9% at baseline to 42 +/- 3.7% (P < 0.01), and diastolic augmentation index (radial pulse) was reduced from 37 +/- 1.8% to 25 +/- 2.9% (P < 0.001). These changes were accompanied by an increase in femoral blood flow (from 409 +/- 44 to 773 +/- 48 ml/min, P < 0.05) and an increase in femoral artery diameter (from 8.2 +/- 0.4 to 8.6 +/- 0.4 mm, P < 0.05). In conclusion, exercise dilates muscular arteries and reduces arterial pressure augmentation, an effect that will enhance ventricular-vascular coupling and reduce load on the left ventricle.AJP Heart and Circulatory Physiology 04/2008; 294(4):H1645-50. DOI:10.1152/ajpheart.01171.2007 · 4.01 Impact Factor