Antoine Yves Marie Guilcher

Coronary and Microvascular Physiology During Intra-Aortic Balloon Counterpulsation

OBJECTIVESnThis study sought to identify the effect of coronary autoregulation on myocardial perfusion during intra-aortic balloon pump (IABP) therapy.nnnBACKGROUNDnIABP is the most commonly used circulatory support device, although its efficacy in certain scenarios has been questioned. The impact of alterations in microvascular function on IABP efficacy has not previously been evaluated in humans.nnnMETHODSnThirteen patients with ischemic cardiomyopathy (left ventricular ejection fraction: 34 ± 8%) undergoing percutaneous coronary intervention were recruited. Simultaneous intracoronary pressure and Doppler-flow measurements were undertaken in the target vessel following percutaneous coronary intervention, during unassisted and IABP-assisted conditions. Coronary autoregulation was modulated by the use of intracoronary adenosine, inducing maximal hyperemia. Wave intensity analysis characterized the coronary wave energies associated with balloon counterpulsation.nnnRESULTSnTwo unique diastolic coronary waves were temporally associated with IABP device use; a forward compression wave and a forward expansion wave caused by inflation and deflation, respectively. During basal conditions, IABP therapy increased distal coronary pressure (82.4 ± 16.1 vs. 88.7 ± 17.8 mm Hg, p = 0.03), as well as microvascular resistance (2.32 ± 0.52 vs. 3.27 ± 0.41 mm Hg cm s(-1), p = 0.001), with no change in average peak velocity (30.6 ± 12.0 vs. 26.6 ± 11.3 cm s(-1), p = 0.59). When autoregulation was disabled, counterpulsation caused an increase in average peak velocity (39.4 ± 10.5 vs. 44.7 ± 17.5 cm s(-1), p = 0.002) that was linearly related with IABP-forward compression wave energy (R(2) = 0.71, p = 0.001).nnnCONCLUSIONSnAutoregulation ameliorates the effect of IABP on coronary flow. However, during hyperemia, IABP augments myocardial perfusion, principally due to a diastolic forward compression wave caused by balloon inflation, suggesting IABP would be of greatest benefit when microcirculatory reserve is exhausted.

Physiology of Angina and its Alleviation with Nitroglycerine- Insights from Invasive Catheter Laboratory Measurements During Exercise

Background: The mechanisms governing exercise-induced angina and its alleviation by the most commonly used antianginal drug, nitroglycerin, are incompletely understood. The purpose of this study was to develop a method by which the effects of antianginal drugs could be evaluated invasively during physiological exercise to gain further understanding of the clinical impact of angina and nitroglycerin. Methods: Forty patients (mean age, 65.2±7.6 years) with exertional angina and coronary artery disease underwent cardiac catheterization via radial access and performed incremental exercise using a supine cycle ergometer. As they developed limiting angina, sublingual nitroglycerin was administered to half the patients, and all patients continued to exercise for 2 minutes at the same workload. Throughout exercise, distal coronary pressure and flow velocity and central aortic pressure were recorded with sensor wires. Results: Patients continued to exercise after nitroglycerin administration with less ST-segment depression (P=0.003) and therefore myocardial ischemia. Significant reductions in afterload (aortic pressure, P=0.030) and myocardial oxygen demand were seen (tension-time index, P=0.024; rate-pressure product, P=0.046), as well as an increase in myocardial oxygen supply (Buckberg index, P=0.017). Exercise reduced peripheral arterial wave reflection (P<0.05), which was not further augmented by the administration of nitroglycerin (P=0.648). The observed increases in coronary pressure gradient, stenosis resistance, and flow velocity did not reach statistical significance; however, the diastolic velocity–pressure gradient relation was consistent with a significant increase in relative stenosis severity (k coefficient, P<0.0001), in keeping with exercise-induced vasoconstriction of stenosed epicardial segments and dilatation of normal segments, with trends toward reversal with nitroglycerin. Conclusions: The catheterization laboratory protocol provides a model to study myocardial ischemia and the actions of novel and established antianginal drugs. Administration of nitroglycerin causes changes in the systemic and coronary circulation that combine to reduce myocardial oxygen demand and to increase supply, thereby attenuating exercise-induced ischemia. Designing antianginal therapies that exploit these mechanisms may provide new therapeutic strategies.

133 Coronary wave intensity: a novel invasive tool for predicting myocardial viability following acute coronary syndromes

Introduction Wave intensity analysis (WIA) uses simultaneous changes in intracoronary pressure and flow to characterise energy transfer within the coronary circulation. In normal hearts, flow is predominantly driven by a microcirculatory-derived, diastolic phase, backward expansion wave (BEW) and aortic-derived, systolic phase, forward compression wave (FCW) (Abstract 133 figure 1A). Regional changes in contraction and microvascular function following acute coronary syndromes (ACS) may affect these waves, but the utility of WIA in this setting remains unknown.Abstract 133 Figure 1 (A) Typical Coronary Wave Intensity Profile. (B) Quantitative LGE Mass and Regional Wall Motion Assessment

41 Reduced arterial wave reflection and enhanced LV relaxation contribute to warm-up angina

Background The mechanisms of the clinically observed phenomenon of reduced angina on second exertion, or warm-up angina, are poorly understood. This study compared changes in central haemodynamics, peripheral wave reflection and patterns of coronary blood flow during serial exercise that may contribute. Methods and Results 16 patients (15 male, 61±4.3u2005yrs) with a positive exercise stress test and exertional angina completed the protocol. During cardiac catheterisation via radial access they performed 2 consecutive exertions (Ex1, Ex2) using a supine cycle ergometer. Throughout exertions, distal coronary pressure (Pd) and flow velocity (V) were recorded in the culprit vessel using a dual sensor coronary guide wire while aortic pressure was recorded using a second wire. Time to 1u2005mm ST depression was longer in Ex2 (p=0.003) and rate pressure product (RPP) was higher (p=0.025) confirming warm-up. A 33% decline in aortic wave reflection (p<0.0001) in Ex2 (see Abstract 41 figure 1A) coincided with a reduction in both tension time index and diastolic time index (p<0.0001). However, the latter was offset by reduced microvascular resistance (Pd/V), p=0.0002, and enhanced left ventricular relaxation during Ex2 as suggested by a larger backward-travelling suction wave (p=0.01) on wave intensity analysis (WIA) of the intra-coronary signals. See Abstract 41 figure 1B. The energy of the forward compression wave and overall coronary blood flow, as measured by the velocity time integral, did not change.Abstract 41 Figure 1 (A) shows aortic pressure traces taken at peak exertion with a reduction in pressure augmentation during Ex2; (B) shows WIA with an increase in the backward expansion, or “sucking” wave originating from the microvasculature. Conclusions In patients with warm-up angina, exercise induces changes in the aortic pressure waveform, microvascular function and LV relaxation. These combine to reduce afterload without compromising myocardial diastolic blood flow thereby likely enabling improved performance on second exercise.

Response to Peripheral Augmentation Index and Wave Reflection in the Radial Artery

We thank Hughes et al1 for their helpful analysis of the relationship between the late systolic shoulder (SBP2) of the peripheral pulse and central systolic blood pressure. Their elegant wave intensity analysis …