Relationship between fiducial points on the peripheral and central blood pressure waveforms: rate of rise of the central waveform is a determinant of peripheral systolic blood pressure.

Central systolic blood pressure (cSBP, the peak of the central waveform) is usually regarded as the determinant of peripheral systolic blood pressure with amplification of peripheral systolic blood pressure (pSBP) measured with reference to cSBP. However, the earlier portion of the central waveform up to the first systolic shoulder (P1) may be the major determinant of pSBP. We performed in silico simulation studies and examined previously acquired experimental data (n = 131) in which peripheral and central blood pressure waveforms had been acquired both invasively and noninvasively to examine the determinants of pSBP. Measurements were made at baseline and during perturbation of hemodynamics by inotropic and vasoactive drugs. In silico simulations using a central-to-peripheral transfer function demonstrated that pSBP is dependent on P1 and the rate of change (dP/dt) of central pressure up to the time of P1 but not cSBP. In computational simulations, peripheral reflection in the radial artery was closely related to dP/dt, and 97% of the variability in amplification as measured with reference to P1 was explained by dP/dt. In vivo, amplification of pSBP over P1 was correlated with dP/dt (R > 0.75, P < 0.0001 for all data sets), and P1 and dP/dt were independently correlated with pSBP, explaining 90% of the variability in pSBP. We conclude that P1 and dP/dt are major determinants of pSBP and that pSBP and cSBP are, in part, determined by different cardiac, central, and peripheral vascular properties.NEW & NOTEWORTHY Peripheral systolic BP is determined mainly by the first shoulder and the rate of rise of the central systolic blood pressure waveform rather than the peak of this waveform (central systolic BP). Peripheral and central systolic blood pressure are determined by different cardiac and vascular properties.

Proficiency of Medical Students at Obtaining Pressure Measurement Readings Using Automated Ankle and Toe Measuring Devices for Diagnosis of Lower Extremity Peripheral Artery Disease.

BACKGROUND: Pressure measurement is a key component in the diagnosis of lower extremity peripheral artery disease (PAD) but is technically challenging and time-consuming for nonvascular specialists, thus hindering its wider implementation. The aim of this study was to assess the proficiency of students at obtaining satisfactory ankle or toe pressure readings for PAD diagnosis using 2 automated devices. METHODS: Medical students followed a training session after which they performed ankle and toe pressure measurements to calculate the ankle-brachial index (ABI) using the MESI ABPI MD® device, and the toe-brachial index (TBI) using the SYSTOE® device. Blinded vascular specialists took the same measurements. Use of the automated devices was considered satisfactory when a valid reading was measured in as few attempts as possible. A comparison was made of each student's proficiency at performing valid ankle and toe pressure measurements. The secondary objective was to compare the readings taken by the vascular specialists with those of the students. RESULTS: Forty-three medical students were included. Mean number of attempts was 1.23 ± 0.48 with the MESI ABPI MD device and 1.44 ± 0.55 with the SYSTOE device (P = 0.04). There was no statistically significant difference between ABI readings taken by the students and those taken by the vascular specialists, 1.17 (0.90; 1.39) vs. 1.18 (0.86; 1.39) (P = 0.33), contrary to TBI readings 0.70 (0.22; 1.74) vs. 0.72 (0.23; 1.16) (P = 0.03). Measurement duration for the students and vascular specialists was 3.75 min ± 1.12 min and 2.26 min ± 0.82 min (P < 0.01) with the MESI ABPI MD device and 4.30 min ± 1.23 min and 3.33 min ± 1.49 min (P = 0.03) with the SYSTOE device. Correlation coefficients between the students and the vascular specialists were 0.56 and 0.34 with the MESI ABPI MD and SYSTOE devices (P < 0.05). CONCLUSIONS: After a brief theoretical training session, the medical students were better at taking ankle pressure measurements than toe pressure measurements with an automated device for the purposes of PAD diagnosis. It would be of value to assess the advantages of these automated devices in primary care practice in future research.

Physiology of Angina and Its Alleviation With Nitroglycerin: 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.

Synergistic adaptations to exercise in the systemic and coronary circulations that underlie the warm-up angina phenomenon.

BACKGROUND: The mechanisms of reduced angina on second exertion in patients with coronary arterial disease, also known as the warm-up angina phenomenon, are poorly understood. Adaptations within the coronary and systemic circulations have been suggested but never demonstrated in vivo. In this study we measured central and coronary hemodynamics during serial exercise. METHODS AND RESULTS: Sixteen patients (15 male, 61±4.3 years) with a positive exercise ECG and exertional angina completed the protocol. During cardiac catheterization via radial access, they performed 2 consecutive exertions (Ex1, Ex2) using a supine cycle ergometer. Throughout exertions, distal coronary pressure and flow velocity were recorded in the culprit vessel using a dual sensor wire while central aortic pressure was recorded using a second wire. Patients achieved a similar workload in Ex2 but with less ischemia than in Ex1 (P<0.01). A 33% decline in aortic pressure augmentation in Ex2 (P<0.0001) coincided with a reduction in tension time index, a major determinant of left ventricular afterload (P<0.001). Coronary stenosis resistance was unchanged. A sustained reduction in coronary microvascular resistance resulted in augmented coronary flow velocity on second exertion (both P<0.001). These changes were accompanied by a 21% increase in the energy of the early diastolic coronary backward-traveling expansion, or suction, wave on second exercise (P<0.05), indicating improved microvascular conductance and enhanced left ventricular relaxation. CONCLUSIONS: On repeat exercise in patients with effort angina, synergistic changes in the systemic and coronary circulations combine to improve vascular-ventricular coupling and enhance myocardial perfusion, thereby potentially contributing to the warm-up angina phenomenon.

Use of a Pre-Trained Neural Network for Automatic Classification of Arterial Doppler Flow Waveforms: A Proof of Concept.

BACKGROUND: Arterial Doppler flow waveform analysis is a tool recommended for the management of lower extremity peripheral arterial disease (PAD). To standardize the waveform analysis, classifications have been proposed. Neural networks have shown a great ability to categorize data. The aim of the present study was to use an existing neural network to evaluate the potential for categorization of arterial Doppler flow waveforms according to a commonly used classification. METHODS: The Pareto efficient ResNet-101 (ResNet-101) neural network was chosen to categorize 424 images of arterial Doppler flow waveforms according to the Simplified Saint-Bonnet classification. As a reference, the inter-operator variability between two trained vascular medicine physicians was also assessed. Accuracy was expressed in percentage, and agreement was assessed using Cohen's Kappa coefficient. RESULTS: After retraining, ResNet-101 was able to categorize waveforms with 83.7 ± 4.6% accuracy resulting in a kappa coefficient of 0.79 (0.75-0.83) (CI 95%), compared with a kappa coefficient of 0.83 (0.79-0.87) (CI 95%) between the two physicians. CONCLUSION: This study suggests that the use of transfer learning on a pre-trained neural network is feasible for the automatic classification of images of arterial Doppler flow waveforms.

Corrigendum: Arterial Doppler Waveforms Are Independently Associated With Maximal Walking Distance in Suspected Peripheral Artery Disease Patients.

[This corrects the article DOI: 10.3389/fcvm.2021.608008.].

Arterial Doppler Waveforms Are Independently Associated With Maximal Walking Distance in Suspected Peripheral Artery Disease Patients.

Objective: Arterial Doppler waveform recordings are commonly used to assess lower extremity arterial disease (LEAD) severity. However, little is known about the relationship between arterial Doppler waveform profiles and patients' walking capacity. The purpose of this study was to assess whether arterial Doppler waveforms are independently associated with maximal walking distance (MWD) in patients experiencing exertional limb symptoms. Materials and Methods: This cross-sectional study included suspected LEAD patients experiencing exertional limb symptoms. In both lower extremities, arterial Doppler waveforms and ankle-brachial index (ABI) values were obtained from the pedis and tibial posterior arteries. Each arterial flow measurement was ranked using the Saint-Bonnet classification system. Treadmill stress testing (3.2 km/h, 10% slope) coupled with exercise oximetry (Exercise-TcPO2) were used to determine MWD. Delta from rest oxygen pressure (DROP) was calculated. Following treadmill stress testing, post-exercise ABI values were recorded. Univariate and multivariate analyses were used to determine the clinical variables associated with MWD. Results: 186 patients experiencing exertional limb symptoms (62 ± 12 years and 26.8 ± 4.5 kg/m2) were included between May 2016 and June 2019. Median [25th; 75th] treadmill MWD was 235 [125;500]m. Better arterial Doppler waveforms were associated with better walking distance (p = 0.0012). Whereas, median MWD was 524 [185;525]m in the group that yielded the best Doppler waveforms, it was 182 [125,305]m in the group with the poorest Doppler waveforms (p = 0.0012). MWD was significantly better (p = 0.006) in the patients with the best ABIs. However, arterial Doppler waveforms alone were significantly associated with MWD (p = 0.0009) in the multivariate model. When exercise variables (post-exercise ABI or DROP) were incorporated into the multivariate model, these were the only variables to be associated with MWD. Conclusion: Of the various clinical parameters at rest, Doppler flow waveform profiles were associated with MWD in suspected LEAD patients. A stronger link was however found between exercise variables and MWD.

Comparison of the Use of Arterial Doppler Waveform Classifications in Clinical Routine to Describe Lower Limb Flow.

BACKGROUND: Characterisation of arterial Doppler waveforms is a persistent problem and a source of confusion in clinical practice. Classifications have been proposed to address the problem but their efficacy in clinical practice is unknown. The aim of the present study was to compare the efficacy of the categorisation rate of Descotes and Cathignol, Spronk et al. and the simplified Saint-Bonnet classifications. METHODS: This is a multicentre prospective study where 130 patients attending a vascular arterial ultrasound were enrolled and Doppler waveform acquisition was performed at the common femoral, the popliteal, and the distal arteries at both sides. Experienced vascular specialists categorized these waveforms according to the three classifications. RESULTS: of 1033 Doppler waveforms, 793 (76.8%), 943 (91.3%) and 1014 (98.2%) waveforms could be categorized using Descotes and Cathignol, Spronk et al. and the simplified Saint-Bonnet classifications, respectively. Differences in categorisation between classifications were significant (Chi squared test, p < 0.0001). Of 19 waveforms uncategorized using the simplified Saint-Bonnet classification, 58% and 84% were not categorized using the Spronk et al. and Descotes and Cathignol classifications, respectively. CONCLUSIONS: The results of the present study suggest that the simplified Saint-Bonnet classification provides a superior categorisation rate when compared with Spronk et al. and Descotes and Cathignol classifications.

Differential effects of beta-adrenoreceptor antagonists on central and peripheral blood pressure at rest and during exercise.

BACKGROUND: Differential effects of beta-adrenoreceptor antagonists (beta-ARB) on central and peripheral blood pressure may relate to change in heart rate and/or vasodilator tone and thus be exaggerated during exercise. AIMS: To examine acute effects of selective and nonselective beta-ARB on central and peripheral blood pressure, cardiac output and peripheral vascular resistance during exercise. METHODS: Healthy volunteers (n= 20, 18 men, 19-54 years) received propranolol 80 mg, bisoprolol 20 mg, and placebo 1 h before bicycle ergometry (50, 75 and 100 W each for 3 min) in a randomized, cross-over study. Cardiac output was determined by pulmonary uptake of soluble and inert gas tracers (InnoCor, Innovision). Central systolic blood pressure (SBP) was determined from the late systolic shoulder of the digital artery pressure waveform (Finometer, Finopres). RESULTS: At rest, both beta-ARB reduced brachial but not central SBP (compared with placebo). During exercise, beta-ARB reduced brachial SBP (reductions of 19.9 +/- 4.3 mmHg and 23.2 +/- 2.7 mmHg for propranolol and bisoprolol, respectively, at 100 W, each P < 0.0001) but not central SBP. The difference between peripheral and central SBP was reduced, relative to that during placebo, by 21.5 mmHg (95% confidence interval 8.8, 34.1) and 26.4 mmHg (18.1, 34.8) for propranolol and bisoprolol, respectively, at 100 W (each P < 0.01). There was no significant effect of beta-ARB on diastolic blood pressure or peripheral vascular resistance. CONCLUSIONS: Despite reducing brachial blood pressure, acute beta-adrenoreceptor blockade in man at rest and during exercise does not reduce central blood pressure.

Effects of Inhibition of Nitric Oxide Synthase on Muscular Arteries During Exercise: Nitric Oxide Does Not Contribute to Vasodilation During Exercise or in Recovery.

Background Basal release of nitric oxide (NO) from the vascular endothelium regulates the tone of muscular arteries and resistance vasculature. Effects of NO on muscular arteries could be particularly important during exercise when shear stress may stimulate increased NO synthesis. Methods and Results We investigated acute effects of NO synthase inhibition on exercise hemodynamics using NG-monomethyl-l-arginine (l-NMMA), a nonselective NO synthase -inhibitor. Healthy volunteers (n=10, 5 female, 19-33 years) participated in a 2-phase randomized crossover study, receiving l-NMMA (6 mg/kg, iv over 5 minutes) or placebo before bicycle exercise (25-150 W for 12 minutes). Blood pressure, cardiac output (measured by dilution of soluble and inert tracers) and femoral artery diameter were measured before, during, and after exercise. At rest, l-NMMA reduced heart rate (by 16.2±4.3 bpm relative to placebo, P<0.01), increased peripheral vascular resistance (by 7.0±1.4 mmHg per L/min, P<0.001), mean arterial blood pressure (by 8.9±3.5 mmHg, P<0.05), and blunted an increase in femoral artery diameter that occurred immediately before exercise (change in diameter: 0.14±0.04 versus 0.32±0.06 mm after l-NMMA and placebo, P<0.01). During/after exercise l-NMMA had no significant effect on peripheral resistance, cardiac output, or on femoral artery diameter. Conclusions These results suggest that NO plays little role in modulating muscular artery function during exercise but that it may mediate changes in muscular artery tone immediately before exercise.

The noninvasive estimation of central aortic blood pressure in patients with aortic stenosis.

OBJECTIVES: To determine the relationship between brachial blood pressure, and transfer function-estimated and invasively measured central aortic pressure in patients with at least moderate symptomatic aortic stenosis. METHODS: Fourteen patients aged 54-81 years with mean (SD) effective valve area of 0.69 (0.20) cm2, undergoing coronary angiography, had simultaneous peripheral and central aortic blood pressure measurements. Brachial blood pressure was determined by an oscillometric method. Aortic pressure was measured directly using pressure transducer tipped catheters, and estimated indirectly by the application of a transfer function to a radial arterial waveform obtained by tonometry. RESULTS: Measured aortic systolic pressure did not differ significantly from brachial pressure [mean difference (SD) 2 (9) mmHg, P = not significant (NS)]. Transfer function estimates of central systolic pressure obtained from the radial waveform calibrated from brachial pressure were less accurate [mean difference -8 (7) mmHg, P = 0.001]. Recalibration of the radial waveforms using the invasive mean and diastolic blood pressure improved the agreement [mean difference -2 (6) mmHg, P = NS] but did not provide a better estimate than brachial blood pressure. The accuracy of noninvasively estimated subendocardial viability ratio was substantially improved by recalibration of radial arterial waveforms using corrected ejection time. CONCLUSION: In patients with aortic stenosis there is clinically acceptable agreement between noninvasive brachial pressure and directly measured central aortic pressure.

Altered dependence of aortic pulse wave velocity on transmural pressure in hypertension revealing structural change in the aortic wall.

Aortic pulse wave velocity (aPWV), a major prognostic indicator of cardiovascular events, may be augmented in hypertension as a result of the aorta being stretched by a higher distending blood pressure or by a structural change. We used a novel technique to modulate intrathoracic pressure and thus aortic transmural pressure (TMP) to examine the variation of intrathoracic aPWV with TMP in hypertensive (n=20; mean±SD age, 52.1±15.3 years; blood pressure, 159.6±21.2/92.0±15.9 mm Hg) and normotensive (n=20; age, 55.5±11.1 years; blood pressure, 124.5±11.9/72.6±9.1 mm Hg) subjects. aPWV was measured using dual Doppler probes to insonate the right brachiocephalic artery and aorta at the level of the diaphragm. Resting aPWV was greater in hypertensive compared with normotensive subjects (897±50 cm/s versus 784±43 cm/s; P<0.05). aPWV was equal in hypertensive and normotensive subjects when measured at a TMP of 96 mm Hg. However, dependence of aPWV on TMP in normotensive subjects was greater than that in hypertensive subjects (9.6±1.6 versus 3.8±0.7 cm/s per mm Hg increase in TMP, respectively, means±SEM; P<0.01). This experimental behavior was best explained by a theoretical model incorporating strain-induced recruitment of stiffer fibers in normotensive subjects and fully recruited stiffer fibers in hypertensive subjects. These results explain previous contradictory findings with respect to isobaric aPWV in hypertensive compared with normotensive subjects. They suggest that hypertension is associated with a profound change in aortic wall mechanical properties possibly because of destruction of elastin leading to less strain-induced stiffening and predisposition to aortic dissection.

Central aortic blood pressure from ultrasound wall-tracking of the carotid artery in children: comparison with invasive measurements and radial tonometry.

Differences between central aortic root (c) and peripheral (p) systolic blood pressure (SBP) may be particularly marked in children, but noninvasive methods for assessing cSBP in children have not been validated. We compared estimates of cSBP obtained from radiofrequency ultrasound wall tracking of the carotid artery (ART.LAB system) with that measured directly by a catheter in the aortic root at the time of arterial cannulation. Carotid waveforms were calibrated from invasive measurements of mean and diastolic pressures. In 9 children aged 10.5 ± 5.0 years (mean ± SD), cSBP obtained from carotid wall tracking was highly correlated with invasive measures of cSBP (r=0.99) with mean (± SD) difference 3.9 ± 2.5 mm Hg. Second, we compared values of cSBP obtained from the carotid with those obtained using noninvasive applanation tonometry at the radial artery and a radial-to-aortic transfer function (SphygmoCor). Both carotid and radial tonometric measurements were calibrated from the same peripheral mean and diastolic measurements of blood pressure obtained by sphygmomanometry. In 84 children aged 13.2 ± 3.2 years, there was excellent agreement between the 2 methods (r=0.95; P<0.001) with mean difference 0.71 ± 3.7 mm Hg (95% confidence interval =-1.53 to 1.01). This invasive validation study confirms that cSBP as estimated by carotid wall tracking provides an acceptable measurement of true cSBP when calibration is from true mean and diastolic pressures. Close agreement of cSBP obtained by carotid wall tracking and radial tonometry suggests that these provide similar results when calibrated from the same peripheral blood pressure measurements.

Augmentation pressure is influenced by ventricular contractility/relaxation dynamics: novel mechanism of reduction of pulse pressure by nitrates.

Augmentation pressure (AP), the increment in aortic pressure above its first systolic shoulder, is thought to be determined mainly by pressure wave reflection but could be influenced by ventricular ejection characteristics. We sought to determine the mechanism by which AP is selectively reduced by nitroglycerin (NTG). Simultaneous measurements of aortic pressure and flow were made at the time of cardiac catheterization in 30 subjects (11 women; age, 61±13 years [mean±SD]) to perform wave intensity analysis and calculate forward and backward components of AP generated by the ventricle and arterial tree, respectively. Measurements were made at baseline and after NTG given systemically (800 µg sublingually, n=20) and locally by intracoronary infusion (1 µg/min; n=10). Systemic NTG had no significant effect on first shoulder pressure but reduced augmentation (and central pulse pressure) by 12.8±3.1 mm Hg (P<0.0001). This resulted from a reduction in forward and backward wave components of AP by 7.0±2.4 and 5.8±1.3 mm Hg, respectively (each P<0.02). NTG had no significant effect on the ratio of amplitudes of either backward/forward waves or backward/forward compression wave energies, suggesting that effects on the backward wave were largely secondary to those on the forward wave. Time to the forward expansion wave was reduced (P<0.05). Intracoronary NTG decreased AP by 8.3±3.6 mm Hg (P<0.05) with no significant effect on the backward wave. NTG reduces AP and central pulse pressure by a mechanism that is, at least in part, independent of arterial reflections and relates to ventricular contraction/relaxation dynamics with enhanced myocardial relaxation.

Dominance of the forward compression wave in determining pulsatile components of blood pressure: similarities between inotropic stimulation and essential hypertension.

Pulsatile components of blood pressure may arise from forward (ventricular generated) or backward wave travel in the arterial tree. The objective of this study was to determine the relative contributions of forward and backward waves to pulsatility. We used wave intensity and wave separation analysis to determine pulsatile components of blood pressure during inotropic and vasopressor stimulation by dobutamine and norepinephrine in normotensive subjects and compared pulse pressure components in hypertensive (mean±SD, 48.8±11.3 years; 165±26.6/99±14.2 mm Hg) and normotensive subjects (52.2±12.6 years; 120±14.2/71±8.2 mm Hg). Dobutamine (7.5 µg/kg per minute) increased the forward compression wave generated by the ventricle and increased pulse pressure from 36.8±3.7 to 59.0±3.4 mm Hg (mean±SE) but had no significant effect on mean arterial pressure or the midsystolic backward compression wave. By contrast, norepinephrine (50 ng/kg per minute) had no significant effect on the forward compression wave but increased the midsystolic backward compression wave. Despite this increase in the backward compression wave, and an increase in mean arterial pressure, norepinephrine increased central pulse pressure less than dobutamine (increases of 22.1±3.8 and 7.2±2.8 mm Hg for dobutamine and norepinephrine, respectively; P<0.02). An elevated forward wave component (mean±SE, 50.4±3.4 versus 35.2±1.8 mm Hg, in hypertensive and normotensive subjects, respectively; P<0.001) accounted for approximately two thirds of the total difference in central pulse pressures between hypertensive and normotensive subjects. Increased central pulse pressure during inotropic stimulation and in essential hypertension results primarily from the forward compression wave.

Coronary and microvascular physiology during intra-aortic balloon counterpulsation.

OBJECTIVES: This study sought to identify the effect of coronary autoregulation on myocardial perfusion during intra-aortic balloon pump (IABP) therapy. BACKGROUND: IABP 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. METHODS: Thirteen 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. RESULTS: Two 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). CONCLUSIONS: Autoregulation 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.

Coronary wave energy: a novel predictor of functional recovery after myocardial infarction.

BACKGROUND: Revascularization after acute coronary syndromes provides prognostic benefit, provided that the subtended myocardium is viable. The microcirculation and contractility of the subtended myocardium affect propagation of coronary flow, which can be characterized by wave intensity analysis. The study objective was to determine in acute coronary syndromes whether early wave intensity analysis-derived microcirculatory (backward) expansion wave energy predicts late viability, defined by functional recovery. METHODS AND RESULTS: Thirty-one patients (58±11 years) were enrolled after non-ST elevation myocardial infarction. Regional left ventricular function and late-gadolinium enhancement were assessed by cardiac magnetic resonance imaging, before and 3 months after revascularization. The backward-traveling (microcirculatory) expansion wave was derived from wave intensity analysis of phasic coronary pressure and velocity in the infarct-related artery, whereas mean values were used to calculate hyperemic microvascular resistance. Twelve-hour troponin T, left ventricular ejection fraction, and percentage late-gadolinium enhancement mass were 1.35±1.21 µg/L, 56±11%, and 8.4±6.0%, respectively. The infarct-related artery backward-traveling (microcirculatory) expansion wave was inversely correlated with late-gadolinium enhancement infarct mass (r=-0.81; P<0.0001) and strongly predicted regional left ventricular recovery (r=0.68; P=0.001). By receiver operating characteristic analysis, a backward-traveling (microcirculatory) expansion wave threshold of 2.8 W m(-2) s(-2)×10(5) predicted functional recovery with sensitivity and specificity of 0.91 and 0.82 (AUC 0.88). Hyperemic microvascular resistance correlated with late-gadolinium enhancement mass (r=0.48; P=0.03) but not left ventricular recovery (r=-0.34; P=0.07). CONCLUSIONS: The microcirculation-derived backward expansion wave is a new index that correlates with the magnitude and location of infarction, which may allow for the prediction of functional myocardial recovery. Coronary wave intensity analysis may facilitate myocardial viability assessment during cardiac catheterization.