Exercise Physiology in the Cath Lab: Still Alive and Well!

Mount Sinai Medical Center, New York, NY.
Circulation (Impact Factor: 14.95). 11/2012; 126(22). DOI: 10.1161/CIRCULATIONAHA.112.146662
Source: PubMed

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: Coronary blood flow peaks in diastole when aortic blood pressure has fallen. Current models fail to completely explain this phenomenon. We present a new approach-using wave intensity analysis-to explain this phenomenon in normal subjects and to evaluate the effects of left ventricular hypertrophy (LVH). We measured simultaneous pressure and Doppler velocity with intracoronary wires in the left main stem, left anterior descending, and circumflex arteries of 20 subjects after a normal coronary arteriogram. Wave intensity analysis was used to identify and quantify individual pressure and velocity waves within the coronary artery circulation. A consistent pattern of 6 predominating waves was identified. Ninety-four percent of wave energy, accelerating blood forward along the coronary artery, came from 2 waves: first a pushing wave caused by left ventricular ejection-the dominant forward-traveling pushing wave; and later a suction wave caused by relief of myocardial microcirculatory compression-the dominant backward-traveling suction wave. The dominant backward-traveling suction wave (18.2+/-13.7 x 10(3) W m(-2)s(-1), 30%) was larger than the dominant forward-traveling pushing wave (14.3+/-17.6 x 10(3) W m(-2) s(-1), 22.3%, P =0.001) and was associated with a substantially larger increment in coronary blood flow velocity (0.51 versus 0.14 m/s, P <0.001). In LVH, the dominant backward-traveling suction wave percentage was significantly decreased (33.1% versus 26.9%, P =0.01) and inversely correlated with left ventricular septal wall thickness (r =-0.52, P <0.02). Six waves predominantly drive human coronary blood flow. Coronary flow peaks in diastole because of the dominance of a "suction" wave generated by myocardial microcirculatory decompression. This is significantly reduced in LVH.
    Circulation 05/2006; 113(14):1768-78. DOI:10.1161/CIRCULATIONAHA.105.603050 · 14.95 Impact Factor
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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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