BackgroundRight ventricular (RV) long-axis function is known to be depressed after cardiac surgery, but the mechanism is not known. We hypothesized that intraoperative transesophageal echocardiography could pinpoint the time at which this happens to help narrow the range of plausible mechanisms.MethodTransthoracic echocardiography was conducted in 33 patients before and after elective coronary artery bypass graft. In an intensively monitored cohort of 9 patients, we also monitored RV function intraoperatively using serial pulsed wave tissue Doppler (PW TD) transesophageal echocardiography.ResultsThere was no significant difference in myocardial velocities from the onset of the operation up to the beginning of pericardial incision, change in RV PW TD S′ velocities 3% ± 2% (P = not significant).Within the first 3 minutes of opening the pericardium, RV PW TD S′ velocities had reduced by 43% ± 17% (P < .001). At 5 minutes postpericardial incision, 2 minutes later, the velocities had more than halved, by 54% ± 11% (P < .0001). Velocities thereafter remained depressed throughout the operation, with final intraoperative S′ reduction being 61% ± 11% (P < .0001).One month after surgery, in the full 33-patient cohort, transthoracic echocardiogram data showed a 55% ± 12% (P < .0001) reduction in RV S′ velocities compared with preoperative values.ConclusionsMinute-by-minute monitoring during cardiac surgery reveals that, virtually, all the losses in RV systolic velocity occurs within the first 3 minutes after pericardial incision. Right ventricular long-axis reduction during coronary bypass surgery results not from cardiopulmonary bypass but rather from pericardial incision.

ObjectivesIn this study, a systematic analysis was conducted of phasic intracoronary pressure and flow velocity in patients with severe aortic stenosis (AS) and coronary artery disease, undergoing transcatheter aortic valve replacement (TAVR), to determine how AS affects: 1) phasic coronary flow; 2) hyperemic coronary flow; and 3) the most common clinically used indices of coronary stenosis severity, instantaneous wave-free ratio and fractional flow reserve.BackgroundA significant proportion of patients with severe aortic stenosis (AS) have concomitant coronary artery disease. The effect of the valve on coronary pressure, flow, and the established invasive clinical indices of stenosis severity have not been studied.MethodsTwenty-eight patients (30 lesions, 50.0% men, mean age 82.1 ± 6.5 years) with severe AS and coronary artery disease were included. Intracoronary pressure and flow assessments were performed at rest and during hyperemia immediately before and after TAVR.ResultsFlow during the wave-free period of diastole did not change post-TAVR (29.78 ± 14.9 cm/s vs. 30.81 ± 19.6 cm/s; p = 0.64). Whole-cycle hyperemic flow increased significantly post-TAVR (33.44 ± 13.4 cm/s pre-TAVR vs. 40.33 ± 17.4 cm/s post-TAVR; p = 0.006); this was secondary to significant increases in systolic hyperemic flow post-TAVR (27.67 ± 12.1 cm/s pre-TAVR vs. 34.15 ± 17.5 cm/s post-TAVR; p = 0.02). Instantaneous wave-free ratio values did not change post-TAVR (0.88 ± 0.09 pre-TAVR vs. 0.88 ± 0.09 post-TAVR; p = 0.73), whereas fractional flow reserve decreased significantly post-TAVR (0.87 ± 0.08 pre-TAVR vs. 0.85 ± 0.09 post-TAVR; p = 0.001).ConclusionsSystolic and hyperemic coronary flow increased significantly post-TAVR; consequently, hyperemic indices that include systole underestimated coronary stenosis severity in patients with severe AS. Flow during the wave-free period of diastole did not change post-TAVR, suggesting that indices calculated during this period are not vulnerable to the confounding effect of the stenotic aortic valve.

Background-Aortic stenosis causes angina despite unobstructed arteries. Measurement of conventional coronary hemodynamic parameters in patients undergoing valvular surgery has failed to explain these symptoms. With the advent of percutaneous aortic valve replacement (PAVR) and developments in coronary pulse wave analysis, it is now possible to instantaneously abolish the valvular stenosis and to measure the resulting changes in waves that direct coronary flow. Methods and Results-Intracoronary pressure and flow velocity were measured immediately before and after PAVR in 11 patients with unobstructed coronary arteries. Using coronary pulse wave analysis, we calculated the intracoronary diastolic suction wave (the principal accelerator of coronary blood flow). To test physiological reserve to increased myocardial demand, we measured at resting heart rate and during pacing at 90 and 120 bpm. Before PAVR, the basal myocardial suction wave intensity was 1.9Ϯ0.3ϫ10 Ϫ5 W ⅐ m Ϫ2 ⅐ s Ϫ2 , and this increased in magnitude with increasing severity of aortic stenosis (rϭ0. 59, Pϭ0.05). This wave decreased markedly with increasing heart rate (␤ coefficientϭϪ0. ; Pϭ0.014). Conclusions-In aortic stenosis, the coronary physiological reserve is impaired. Instead of increasing when heart rate rises, the coronary diastolic suction wave decreases. Immediately after PAVR, physiological reserve returns to a normal positive pattern. This may explain how aortic stenosis can induce anginal symptoms and their prompt relief after PAVR. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01118442. Key Words: aortic stenosis Ⅲ aortic valve Ⅲ coronary arteries Ⅲ coronary flow Ⅲ heart valve prosthesis implantation Ⅲ microvessels Ⅲ wavelet analysis U ncorrected severe aortic stenosis has an extremely poor prognosis, carrying a 3-year mortality of Ͼ50%, 1 which rises to Ͼ80% in subjects with significant cardiac comorbidity. 2 As the severity of aortic stenosis increases, physiological and pathological adaptations occur in the left ventricle (LV). 3 These include increases in the inotropic state and the development of LV hypertrophy. 4 Editorial see p 1505 Clinical Perspective on p 1572Although LV hypertrophy can be viewed as a physiological adaptation to the increase in afterload, it encompasses a pathological hypertrophic response with increased extracellular matrix deposition and perivascular fibrosis. 5 These pathological changes slow myocardial relaxation, which in turn diminishes normal ventricular filling and reduces coronary blood flow. 6,7 This is compounded by the increase in work and myocardial mass, which results in elevated myocardial oxygen demand and a decrease in microvascular density, 8 leading to reduced coronary vascular reserve. 9 As the severity of the aortic stenosis increases, this process is exacerbated by ever-increasing afterload and decreasing coronary perfusion pressures, leading to the development of ischemia, which has been reported with the use of several different techniques. 10...