Suction Wave Research Articles

Mechanisms of gradual pressure drop in angiographically normal left anterior descending and right coronary artery: Insights from wave intensity analysis

BackgroundThis study evaluated the mechanism of decline in coronary pressure from the proximal to the distal part of the coronary arteries in the left anterior descending (LAD) versus the right coronary artery (RCA) from the insight of coronary hemodynamics using wave intensity analysis (WIA). MethodsTwelve patients with angiographically normal LAD and RCA were prospectively enrolled. Distal coronary pressure, mean aortic pressure, and average peak velocity were measured at 4 different positions: 9, 6, 3, and 0 cm distal from each coronary ostium. ResultsThe distal-to-proximal coronary pressure ratio during maximum hyperemia gradually decreased in proportion to the distance from the ostium (0.92±0.03 and 0.98±0.03 at 9 cm distal to the LAD and RCA ostium). WIA showed the dominant forward-traveling compression wave gradually decreased and the backward-traveling suction wave gradually decreased in proportion to the decrease in coronary pressure through the length of the non-diseased LAD but not the RCA. ConclusionsThe pushing wave and suction wave intensities on WIA were diminished in proportion to the distance from the ostium of the LAD despite the wave intensity not changing across the length of the RCA, which may lead to gradual intracoronary pressure drop in the angiographically normal LAD.

Coronary wave intensity patterns in stable coronary artery disease: influence of stenosis severity and collateral circulation

ObjectiveWave intensity analysis is a method that allows separating pulse waves into components generated proximally and in the periphery of arterial trees, as well as characterising them as accelerating or...

A unified mechanism for the water hammer pulse and pulsus bisferiens in severe aortic regurgitation: Insights from wave intensity analysis

The carotid bisferiens pulse and the radial water hammer pulse are typical of severe chronic aortic regurgitation. Little is known about the mechanism of these classic cardiovascular signs identified on physical examination. We report the first characterization of these abnormal pulse patterns using wave intensity analysis (WIA) in a patient with severe aortic regurgitation. We demonstrate that an abnormally pronounced forward-traveling mid-systolic suction wave, which immediately followed the initial forward-traveling compression wave from ventricular contraction, explained these pulse patterns. This suction wave likely resulted from blood inertia, arising from a ventricle ejecting a very large stroke volume into a vasodilated arterial tree. Our report demonstrates a novel pulsatile hemodynamic mechanism that unifies the pathogenesis of the bisferiens pulse and the water-hammer pulse in severe aortic regurgitation.

Diastolic Backward-Traveling Decompression (Suction) Wave Correlates With Simultaneously Acquired Indices of Diastolic Function and Is Reduced in Left Ventricular Stunning.

Wave intensity analysis can distinguish proximal (propulsion) and distal (suction) influences on coronary blood flow and is purported to reflect myocardial performance and microvascular function. Quantifying the amplitude of the peak, backwards expansion wave (BEW) may have clinical utility. However, simultaneously acquired wave intensity analysis and left ventricular (LV) pressure-volume loop data, confirming the origin and effect of myocardial function on the BEW in humans, have not been previously reported. Patients with single-vessel left anterior descending coronary disease and normal ventricular function (n=13) were recruited prospectively. We simultaneously measured LV function with a conductance catheter and derived wave intensity analysis using a pressure-low velocity guidewire at baseline and again 30 minutes after a 1-minute coronary balloon occlusion. The peak BEW correlated with the indices of diastolic LV function: LV dP/dtmin (rs=-0.59; P=0.002) and τ (rs=-0.59; P=0.002), but not with systolic function. In 12 patients with paired measurements 30 minutes post balloon occlusion, LV dP/dtmax decreased from 1437.1±163.9 to 1299.4±152.9 mm Hg/s (median difference, -110.4 [-183.3 to -70.4]; P=0.015) and τ increased from 48.3±7.4 to 52.4±7.9 ms (difference, 4.1 [1.3-6.9]; P=0.01), but basal average peak coronary flow velocity was unchanged, indicating LV stunning post balloon occlusion. However, the peak BEW amplitude decreased from -9.95±5.45 W·m(-2)/s(2)×10(5) to -7.52±5.00 W·m(-2)/s(2)×10(5) (difference 2.43×10(5) [0.20×10(5) to 4.67×10(5); P=0.04]). Peak BEW assessed by coronary wave intensity analysis correlates with invasive indices of LV diastolic function and mirrors changes in LV diastolic function confirming the origin of the suction wave. This may have implications for physiological lesion assessment after percutaneous coronary intervention. URL: http://www.isrctn.org. Unique identifier: ISRCTN42864201.

In silico coronary wave intensity analysis: application of an integrated one-dimensional and poromechanical model of cardiac perfusion.

Coronary wave intensity analysis (cWIA) is a diagnostic technique based on invasive measurement of coronary pressure and velocity waveforms. The theory of WIA allows the forward- and backward-propagating coronary waves to be separated and attributed to their origin and timing, thus serving as a sensitive and specific cardiac functional indicator. In recent years, an increasing number of clinical studies have begun to establish associations between changes in specific waves and various diseases of myocardium and perfusion. These studies are, however, currently confined to a trial-and-error approach and are subject to technological limitations which may confound accurate interpretations. In this work, we have developed a biophysically based cardiac perfusion model which incorporates full ventricular–aortic–coronary coupling. This was achieved by integrating our previous work on one-dimensional modelling of vascular flow and poroelastic perfusion within an active myocardial mechanics framework. Extensive parameterisation was performed, yielding a close agreement with physiological levels of global coronary and myocardial function as well as experimentally observed cumulative wave intensity magnitudes. Results indicate a strong dependence of the backward suction wave on QRS duration and vascular resistance, the forward pushing wave on the rate of myocyte tension development, and the late forward pushing wave on the aortic valve dynamics. These findings are not only consistent with experimental observations, but offer a greater specificity to the wave-originating mechanisms, thus demonstrating the value of the integrated model as a tool for clinical investigation.

TCT-287 The diastolic backwards-travelling decompression “suction” wave correlates with simultaneously acquired indices of diastolic function: corroboration of the origin of the suction wave

TCT-287 The diastolic backwards-travelling decompression “suction” wave correlates with simultaneously acquired indices of diastolic function: corroboration of the origin of the suction wave

Abstract 19263: Vasodilator Use and Wave Intensity Patterns in Hypertension

Background: Blood pressure is the result of interactions between the heart and the arteries. Although the effects of vasoactive blood pressure-lowering drugs on arteries has been widely investigated, their in vivo effects on ventricular-arterial interactions are not well understood. Hypothesis: We aimed to assess the relationship between antihypertensive drug use and ventricular arterial interactions assessed via wave intensity analysis (WIA), which quantifies the energy contained in waves generated by the heart and/or reflected from the periphery (figure). Methods: We studied 152 subjects with treated hypertension. We measured central pressure using carotid arterial tonometry. Ascending aortic flow was quantified with through-plane phase-contrast MRI. We performed WIA and assessed the relationship between specific classes of blood pressure lowering drug use and WIA patterns. Results: In models that adjusted for age, gender, body size, race, presence of diabetes and glomerular filtration rate, angiotensin receptor blocker (ARB) use was associated with a greater likelihood of a mid-systolic expansion (i.e., suction) wave (Hazard Ratio=31.1; P=0.005), whereas beta-blocker use was associated with a lower likelihood of such wave (HR=0.16; P=0.02). ARB use was also independently associated with a lower energy in the late systolic forward suction wave (Beta=-0.18; standardized beta=-0.24; P=0.007). This association persisted after adjustment for the forward compression wave (beta=-0.13; standardized beta=-0.16; P=0.008). No associations between WIA patterns and calcium channel blocker use, diuretic use, ACE inhibitor use or long-anting nitrate use were found. Conclusions: Wave intensity analysis is a useful tool to assess the effects of vasodilators on ventricular-arterial interactions. ARB use is selectively associated with systolic suction waves (from blood inertia), which may in turn unload the heart in mid and late systole.

Circulation Editors’ Picks

<i>Circulation</i> Editors’ Picks

Destruction Analysis of Broadside Multi-Cabin Protective Structure of Warship under Explosion Loading

Shock wave parameters of cabins for shipboard defensive structure are studied based on shock wave theory. The destroy of defensive structure can be estimated by impulse of shock wave. In the process of air shock wave propagating, isentropic suction wave is reflected from void cabin into defense structure. The solution of shock wave attenuation of void cabin can be reached by using isentropic line to replace the shock adiabatic of the reflected shock. It can be seen from the example that the multi-layers defense structure system of warship is very important to decrease the damage from explosive shock wave. The method can be used to predict the extent of damage of naval vessel.

First-in-man evidence of the mechanistic effects of biventricular pacing on coronary physiology

BackgroundNormal coronary blood flow is principally determined by a diastolic backward travelling decompression (suction) wave. Dyssynchronous heart failure may attenuate suction. We hypothesised that biventricular pacing, by restoring left ventricular (LV) synchronisation and improving LV relaxation, might increase this suction wave and coronary flow. MethodsTen patients with congestive heart failure (nine men; mean age 65 years [SD 12]; mean ejection fraction 26% [SD 7] with left bundle branch block (LBBB, mean QRS duration 174 ms [SD 18]) underwent atriobiventricular pacing at 100 beats per min. LV pressure was measured and wave intensity calculated from invasive coronary flow velocity and pressure, with native conduction (LBBB) and during biventricular pacing at atrioventricular (AV) delays of 40 ms (BiV-40), 120 ms (BiV-120), and separately pre-identified haemodynamically optimal AV delay (BiV-Opt). Data are given as median (IQR). FindingsCompared with LBBB, BiV-Opt enhanced coronary flow velocity time integral (VTI) by 15% (7–25, p=0·007), LV dP/dtmax by 17% (9–22, p=0·005), and negdP/dtmax by 17% (9–22, p=0·005). The cumulative intensity of the diastolic backward decompression (suction) wave increased by 26% (18–54, p=0·005). Much of the increase in coronary flow VTI occurred in diastole (69% [41–84], p=0·047). The systolic compression waves also increased: forward by 36% (6–49; p=0·022) and backward by 38% (20–55, p=0·022). BiV-120 generated a smaller LV dP/dtmax (by 12% [5–23], p=0·013) and negdP/dtmax (by 15% [8–40], p=0·009) increase than did BiV-OPT, with LBBB as reference; BiV-Opt and BiV-120 were not significantly different in coronary flow VTI or waves. BiV-40 was no different from LBBB. InterpretationWhen biventricular pacing improves left ventricular contraction and relaxation, it increases coronary blood flow velocity, predominantly by increasing the dominant diastolic backward decompression wave. FundingBritish Heart Foundation.

Improvement in Coronary Blood Flow Velocity With Acute Biventricular Pacing Is Predominantly Due to an Increase in a Diastolic Backward-Travelling Decompression (Suction) Wave

Normal coronary blood flow is principally determined by a backward-traveling decompression (suction) wave in diastole. Dyssynchronous chronic heart failure may attenuate suction, because regional relaxation and contraction overlap in timing. We hypothesized that biventricular pacing, by restoring left ventricular (LV) synchronization and improving LV relaxation, might increase this suction wave, improving coronary flow. Ten patients with chronic heart failure (9 males; age 65±12; ejection fraction 26±7%) with left bundle-branch block (LBBB; QRS duration 174±18 ms) were atriobiventricularly paced at 100 bpm. LV pressure was measured and wave intensity calculated from invasive coronary flow velocity and pressure, with native conduction (LBBB) and during biventricular pacing at atrioventricular (AV) delays of 40 ms, 120 ms, and separately preidentified hemodynamically optimal AV delay. In comparison with LBBB, biventricular pacing at separately preidentified hemodynamically optimal AV delay (BiV-Opt) enhanced coronary flow velocity time integral by 15% (7%-25%) (P=0.007), LV dP/dt(max) by 15% (10%-21%) (P=0.005), and (neg)dP/dt(max) by 17% (9%-22%) (P=0.005). The cumulative intensity of the diastolic backward decompression (suction) wave increased by 26% (18%-54%) (P=0.005). The majority of the increase in coronary flow velocity time integral occurred in diastole (69% [41%-84% ]; P=0.047). The systolic compression waves also increased: forward by 36% (6%-49%) (P=0.022) and backward by 38% (20%-55%) (P=0.022). Biventricular pacing at AV delays of 120 ms generated a smaller LV dP/dt(max) (by 12% [5%-23% ], P=0.013) and (neg)dP/dt(max) (by 15% [8%-40% ]; P=0.009) increase than BiV-Opt, against LBBB as reference; BiV-Opt and biventricular pacing at AV delays of 120 ms were not significantly different in coronary flow velocity time integral or waves. Biventricular pacing at AV delays of 40 ms was no different from LBBB. When biventricular pacing improves LV contraction and relaxation, it increases coronary blood flow velocity, predominantly by increasing the dominant diastolic backward decompression (suction) wave.

Percutaneous Coronary Intervention (PCI) Enhances the Amplitude of the Early Diastolic Suction Wave in the Treated Artery

Background: Coronary flow is critically dependent on suction developed by the myocardium in diastole and left ventricular ejection during systole, both of which accelerate flow. Wave intensity analysis enables quantification and separation of these forces. The impact of (PCI) on the coronary wave intensity (CWI) profile is unclear. Methods: We performed simultaneous intracoronary pressure and velocity measurements in 17 patients undergoing elective PCI. Measurements were made distal to the target lesion prior to and following PCI during adenosine induced hyperaemia. Coronary wave speed (SPc) was calculated utilising the “single point sum-of-squares” method. Wave intensity profiles of ensemble averaged cardiac cycles were constructed applying previously described equations. The peak intensities of the dominant forward travelling “pushing” wave (Wave 2) and the dominant backward travelling “suction” wave (Wave 5) were calculated prior to and following PCI. Results: CWI profiles demonstrated the previously described six major waves. PCI resulted in substantial increases in peak intensity of Wave 2 and Wave 5 (mean increases in peak intensity of 227% p = 0.0007 and 170% p = 0.0005, respectively). Significant decreases were seen in SPc distal to the lesion following PCI (p = 0.003) and with intracoronary adenosine (p = 0.0003). Conclusion: PCI appears to augment both the forward travelling “pushing” wave and backward travelling “suction” waves. These findings are consistent with the enhancement of coronary flow seen with PCI. The decrease in wave speed following PCI and intracoronary adenosine may be explained by an increase in coronary diameter induced by increased flow.

Arterial Pulse Wave Dynamics After Percutaneous Aortic Valve Replacement

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 1.9±0.3×10 −5 W · m −2 · s −2 , and this increased in magnitude with increasing severity of aortic stenosis ( r =0.59, P =0.05). This wave decreased markedly with increasing heart rate (β coefficient=−0.16×10 −4 W · m −2 · s −2 ; P &lt;0.001). After PAVR, despite a fall in basal suction wave (1.9±0.3 versus 1.1±0.1×10 −5 W · m −2 · s −2 ; P =0.02), there was an immediate improvement in coronary physiological reserve with increasing heart rate (β coefficient=0.9×10 −3 W · m −2 · s −2 ; P =0.014). 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.

Changing Reflections of the Coronary Microcirculation After Percutaneous Aortic Valve Replacement

In this issue of Circulation , Davies et al1 assess the changes in coronary blood flow and reserve after the relief of aortic stenosis (AS) by percutaneous aortic valve replacement (PAVR) and implicate these findings as additional mechanisms bearing on the critical role of the coronary microcirculation in this population. Article see p 1565 One cannot help but be intrigued by the novel physiological insights that pulsed wave analysis brings to one of the oldest cardiovascular diseases, AS, and one of the newest procedures in interventional cardiology, namely PAVR. For decades, the diagnosis and treatment of AS have rightly focused on identifying and then ameliorating the adverse consequences of abnormal transvalvular pressure and flow. In the absence of coronary artery disease, the mechanisms of angina in AS were debated and attributed mostly to microvascular insufficiency with ischemia resulting from myocardial oxygen supply/demand imbalance. Left ventricular (LV) muscle mass was increased out of proportion to myocardial capillary oxygen supply.2,3 As one might expect in medical science, this is not the end of the story. Examining the arterial pulsed wave dynamics that characterize features of both epicardial and microcirculatory blood flow, Davies et al detail additional mechanisms beyond coronary reserve impairment to better understand why angina may occur in the AS patient with normal coronary arteries. PAVR produced not only a fall in myocardial microvascular resistance, but also improved diastolic filling waves related to favorable changes in LV wall stress as another postulated mechanism for a reduction in …

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

BackgroundThe 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...

099 Acute changes in coronary haemodynamic in patients undergoing transcatheter aortic valve implantation

<h3>Introduction</h3> Aortic stenosis (AS) and left ventricular hypertrophy (LVH) detrimentally alter coronary haemodynamics and increase mortality. However, it has never been possible to discriminate between the effects of severe left ventricular pressure loading and chronic changes of LVH. We assessed this invasively in subjects before and immediately after transcatheter aortic valve implantation (TAVI). <h3>Methods</h3> In 26 subjects (35–91years) coronary artery pressure and flow velocity were measured using intra-arterial wires. 3 cohorts with unobstructed arteries were assessed: (1) No LVH (n=10), (2) LVH (n=11), and (3) AS and LVH undergoing TAVI (n=6). To quantify the effects that pressure loading and LVH have on coronary haemodynamics wave separation was performed using wave intensity analysis, and physiological reserve assessed by pacing <h3>Results</h3> In subjects without AS, LVH was associated with a reduction in myocardial suction wave (6.1±4 v 3.1±2×10⁻⁵ Wm⁻² s⁻¹, p=0.03). In TAVI subjects this wave was lower in comparison to LVH group (2.2±1×10⁻⁵ Wm⁻² s⁻¹, p&lt;0.001), and decreased further with pacing (90 bpm;1.2±0.6 and 120bpm;1.2±0.7 x10⁻⁵ Wm⁻²s⁻¹ respectively p=0.03 for both). Post-TAVI the suction wave fell markedly (2.2±1 v 0.8±0.5×10–5 Wm⁻² s⁻¹, p=0.01) below that seen in subjects with unobstructed arteries and LVH without AS (3.1±2×10⁻⁵ Wm⁻² s⁻¹, p&lt;0.01). <h3>Conclusions</h3> Aortic stenosis and LVH are independently detrimental to coronary haemodynamics. Despite relief of aortic obstruction coronary haemodynamics remains impaired after TAVI probably due to the deleterious effects of severe LVH. With regression of LVH after successful treatment, normalisation may occur.

Differences in cardiac microcirculatory wave patterns between the proximal left mainstem and proximal right coronary artery

Despite having almost identical origins and similar perfusion pressures, the flow-velocity waveforms in the left and right coronary arteries are strikingly different. We hypothesized that pressure differences originating from the distal (microcirculatory) bed would account for the differences in the flow-velocity waveform. We used wave intensity analysis to separate and quantify proximal- and distal-originating pressures to study the differences in velocity waveforms. In 20 subjects with unobstructed coronary arteries, sensor-tipped intra-arterial wires were used to measure simultaneous pressure and Doppler velocity in the proximal left main stem (LMS) and proximal right coronary artery (RCA). Proximal- and distal-originating waves were separated using wave intensity analysis, and differences in waves were examined in relation to structural and anatomic differences between the two arteries. Diastolic flow velocity was lower in the RCA than in the LMS (35.1 +/- 21.4 vs. 56.4 +/- 32.5 cm/s, P < 0.002), and, consequently, the diastolic-to-systolic ratio of peak flow velocity in the RCA was significantly less than in the LMS (1.00 +/- 0.32 vs. 1.79 +/- 0.48, P < 0.001). This was due to a lower distal-originating suction wave (8.2 +/- 6.6 x 10(3) vs. 16.0 +/- 12.2 x 10(3) W.m(-2).s(-1), P < 0.01). The suction wave in the LMS correlated positively with left ventricular pressure (r = 0.6, P < 0.01) and in the RCA with estimated right ventricular systolic pressure (r = 0.7, P = 0.05) but not with the respective diameter in these arteries. In contrast to the LMS, where coronary flow velocity was predominantly diastolic, in the proximal RCA coronary flow velocity was similar in systole and diastole. This difference was due to a smaller distal-originating suction wave in the RCA, which can be explained by differences in elastance and pressure generated between right and left ventricles.

Abstract 3351: The Coronary Suction Wave in Humans Is Not Diminished by Ischemia Induced Left Ventricular Diastolic Dysfunction.

Background: A dominant suction wave due to ventricular relaxation has been postulated to contribute to normal coronary artery flow. We hypothesised that this wave would: be present in diseased coronary arteries, occur at the appropriate time in the cardiac cycle and be diminished following coronary artery balloon occlusion due to ischemia induced diastolic LV dysfunction. Methods: Simultaneous coronary pressure - velocity and LV pressure - volume were invasively recorded at baseline and after 1 minute coronary balloon occlusion, in 10 patients with single vessel coronary disease and normal LV function. Net coronary wave intensity (WI) = (dP/dt).(dU/dt) was calculated using MatLab software. Results: A dominant forward pushing wave and a backward suction wave (figure - shaded wave) were demonstrated in diseased coronary arteries. The suction wave occurred early in diastole, during active ventricular relaxation. Ischemia induced LV diastolic dysfunction was demonstrated after coronary artery occlusion (mean % Δ from baseline (SD): LV dP/dt min = −14.8 (13.8), p=0.008, LV Tau = +19.1(14.9), p = 0.011) but there was no significant change in suction WI (mean (SD): baseline = −1.35 (0.20) m −2 s −2 x10 5 , post-balloon occlusion −1.49(0.59) m −2 s −2 x10 5 , p =0.67). Conclusion: The coronary suction wave occurs in diseased coronary arteries at the appropriate time in the cardiac cycle but is not diminished by ischemia induced diastolic left ventricular dysfunction.

Evidence of a Dominant Backward-Propagating “Suction” Wave Responsible for Diastolic Coronary Filling in Humans, Attenuated in Left Ventricular Hypertrophy

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.

1092 The effects of age and hypertension on the protodiastolic left ventricular suction wave measured using wave intensity analysis

1092 The effects of age and hypertension on the protodiastolic left ventricular suction wave measured using wave intensity analysis