Coronary wave intensity during the Valsalva manoeuvre in humans reflects altered intramural vessel compression responsible for extravascular resistance.

Our aim was to investigate the effect of altered cardiac-coronary interaction during the Valsalva manoeuvre (VM) on coronary wave intensity and the response of coronary microvascular resistance. In 13 patients, left ventricular (P(LV)) and aortic pressure were measured during catheterization, together with intracoronary pressure and blood flow velocity (U) via a dual-sensor guide wire advanced into an angiographically normal coronary artery. Signals were analysed for the following phases of VM: baseline (B1), onset of strain (S1), sustained strain (S2), onset of release (R1), maximal response during recovery (R2), and baseline after VM. The immediate effects of VM were most evident from diastolic P(LV) (LVDP), which increased from 11.0 ± 2.3 to 36.4 ± 2.7 mmHg between B1 and S1 and fell from 28.3 ± 3.4 to 8.3 ± 1.9 mmHg between S2 and R1. Wave intensities and rate pressure product (RPP) were only minimally affected at these transient phases, but coronary wave energies decreased by about 50% and RPP by 38% from S1 to S2, together with a 30% depression of LVdP/dt. All signals were restored to baseline values during the recovery. U did not vary significantly throughout the VM. Despite the depressed cardiac performance during VM strain, microvascular resistance, calculated with LVDP as backpressure, decreased by 31% from B1 to S2, whereas an increase via metabolically induced vasoconstriction was expected. Since coronary U remained essentially constant despite the marked reduction in oxygen consumption, microvascular vasoconstriction must have been compensated by a decrease in the contraction-mediated impediment on coronary blood flow, as confirmed by the reduced coronary wave energies.

Acute haemodynamic effects of accelerated idioventricular rhythm in primary percutaneous coronary intervention.

AIMS: Accelerated idioventricular rhythm (AIVR) is very frequently observed in primary percutaneous coronary intervention (PCI), however knowledge of the haemodynamic effects is lacking. METHODS AND RESULTS: We studied an ST-segment elevation myocardial infarction cohort of 128 consecutive patients (aged 62±11 years) in whom AIVR occurred following reperfusion during primary PCI. Mean systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate were determined during periods of AIVR and sinus rhythm. We grouped patients according to the infarct-related artery and the site of the coronary occlusion. AIVR caused an immediate reduction in SBP (130±27 vs. 98±22 mmHg, p<0.001) and DBP (80±19 vs. 69±16 mmHg, p<0.001) and a small increase in heart rate (78±12 vs. 83±11 bpm, p<0.001) as compared to sinus rhythm, irrespective of infarct-related artery. Both absolute as well as relative reduction in SBP were more pronounced in distal than proximal left coronary artery (LCA) occlusions (36±16 vs. 27±12 mmHg, p<0.01, respectively 25±9 vs. 20±8%, p<0.05). These haemodynamic differences between proximal and distal occlusion sites were not observed in the right coronary artery. CONCLUSIONS: AIVR following reperfusion is associated with marked reduction in both SBP and DBP, irrespective of infarct-related artery. These haemodynamic effects are accompanied by only a very modest increase in heart rate during AIVR. Patients with a culprit lesion in the proximal LCA showed a smaller reduction in systolic blood pressure than distal LCA lesions.

Right ventricular pacing improves haemodynamics in right ventricular failure from pressure overload: an open observational proof-of-principle study in patients with chronic thromboembolic pulmonary hypertension.

AIMS: Right ventricular (RV) failure in patients with chronic thromboembolic pulmonary hypertension (CTEPH), and other types of pulmonary arterial hypertension is associated with right-to-left ventricle (LV) delay in peak myocardial shortening and, consequently, the onset of diastolic relaxation. We aimed to establish whether RV pacing may resynchronize the onsets of RV and LV diastolic relaxation, and improve haemodynamics. METHODS AND RESULTS: Fourteen CTEPH patients (mean age 63.7 ± 12.0 years, 10 women) with large (≥60 ms) RV-to-LV delay in the onset of diastolic relaxation (DIVD, diastolic interventricular delay) were studied. Temporary RV pacing was performed by atrioventricular (A-V) sequential pacing with incremental shortening of A-V delay to advance RV activation. Effects were assessed using tissue Doppler echocardiography and LV pressure-conductance catheter measurements in a subset of patients. Compared with right atrial pacing, RV pacing at optimal A-V delay (average 140 ± 22 ms, range 120-180 ms) resulted in significant DIVD reduction (59 ± 19 to 3 ± 22 ms, P < 0.001), and increase in LV stroke volume as measured by LV outflow tract velocity-time integral (14.9 ± 2.8 to 16.9 ± 3.0 cm, P < 0.001), along with enhanced global RV contractility and LV diastolic filling. CONCLUSION: Right-to-left ventricle resynchronization of the onset of diastolic relaxation results in stroke volume increase in CTEPH patients. Whether RV pacing may be a novel therapeutic target in RV failure following chronic pressure overload remains to be investigated.

Long-term safety and sustained left ventricular recovery: long-term results of percutaneous left ventricular support with Impella LP2.5 in ST-elevation myocardial infarction.

AIMS: Mechanical left ventricular (LV) unloading may reduce infarct size when combined with primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). The Impella LP2.5 is a novel percutaneous left ventricular assist device. Although the short-term safety and feasibility of this device have been demonstrated, the long-term effects are unknown. The purpose of the current study was to evaluate the long-term effects of the Impella LP2.5 support on the aortic valve and left ventricular ejection fraction (LVEF). METHODS AND RESULTS: In 2006, 10 patients with anterior STEMI received 3-day support with the Impella LP2.5 after PCI. The control group consisted of 10 comparable patients, treated according to routine care. For the current study, echocardiography was performed and adverse events were recorded. Mean duration of follow-up was 2.9±0.6 years in the Impella group and 3.0±0.3 years in the control group. No differences in aortic valve abnormalities and LVEF were demonstrated between the groups; nevertheless, LVEF increase from baseline was significantly greater in Impella-treated patients (23.6±8.9% versus 6.7±7.0%, P=0.008). CONCLUSIONS: Three-day support with the Impella LP2.5 is not associated with adverse effects on the aortic valve at long-term follow-up. LVEF was similar in both groups; however, recovery was significantly greater in the Impella group.

More pronounced diastolic left ventricular dysfunction in patients with accelerated idioventricular rhythm after reperfusion by primary percutaneous coronary intervention.

OBJECTIVE: Reperfusion-induced accelerated idioventricular rhythm (AIVR) during primary percutaneous coronary intervention (pPCI) may be a sign of left ventricular (LV) dysfunction. We compared LV dynamic effects of reperfusion between patients with and without reperfusion-induced AIVR during pPCI for ST-elevation myocardial infarction (STEMI). METHODS: We studied 15 consecutive patients, who presented with their first acute anterior STEMI within 6 hours after onset of symptoms, and in whom LV pressure-volume (PV) loops were directly obtained during pPCI. Immediate effects of pPCI on LV function were compared between patients with (n = 5) and without (n = 10) occurrence of AIVR after reperfusion, as well as the direct effects of AIVR on LV function compared to sinus rhythm. RESULTS: Patients with reperfusion-induced AIVR showed more pronounced diastolic LV dysfunction before the onset of the arrhythmia, i.e., a delayed active relaxation expressed by Tau (53 ± 15 vs. 39 ± 6 ms; p = 0.03), a worse compliance curve (p = 0.01), and a higher end-diastolic stiffness (p = 0.07). At the end of the procedure, AIVR patients showed less improvement in diastolic LV function, indicated by a downward shift of the compliance curve (-3.1 ± 2.3 vs. -7.5 ± 1.4 mmHg; p = 0.001), a decrease in end-diastolic stiffness (13 ± 18 vs. 34 ± 15%; p = 0.03) and end-diastolic pressure (12 ± 8 vs. 29 ± 19%; p = 0.07). CONCLUSION: STEMI patients with reperfusion-induced AIVR after pPCI showed more pronounced diastolic LV dysfunction before and after AIVR than patients without AIVR, which suggests that diastolic LV dysfunction contributes to the occurrence of AIVR and that AIVR is a sign of diastolic LV dysfunction.

Effect of the Valsalva maneuver on cardiac-coronary interaction assessed by wave intensity analysis.

The Valsalva maneuver (VM) provokes strong changes in the cardiovascular system and is therefore well suited to study the cardiac-coronary interaction in humans. In 12 patients undergoing catheterization we simultaneously recorded aortic pressure, left ventricular pressure, and intracoronary pressure (Pd) and flow velocity (U) while the patients were performing a VM. Coronary wave intensity was calculated (dI = dP*dU) at characteristic phases of the VM and related to hemodynamic parameters of left ventricular (LV) performance. During the strain, blood pressure increased transiently followed by a significant decrease (p < 0.001) at maximum strain. Changes in mean LV pressure followed the same pattern, while LV end-diastolic pressure increased to almost 40 mmHg (p < 0.001), with a 30% reduction in LV dP/dt (p < 0.005). Coronary flow velocity remained fairly constant throughout the VM. All hemodynamic values returned to the baseline at conclusion of the maneuver. Coronary wave intensity was strongly reduced during the strain and was related to the depression in LV performance. Wave intensity analysis clearly revealed the inherent features of cardiac-coronary interaction.

The effect of repeated ischaemic periods on left ventricular dynamics during percutaneous coronary intervention.

AIMS: To study online left ventricular (LV) dynamic effects of transmural ischaemia and reperfusion during consecutive balloon coronary occlusions in the setting of percutaneous coronary intervention (PCI). METHODS AND RESULTS: In 10 consecutive unselected patients with stable angina (seven males, mean age 62 ± 3 years) who underwent elective PCI, LV dynamics were continuously recorded using a pressure-conductance catheter to simultaneously measure pressure and volume (PV-loop). The effects of a prolonged balloon coronary occlusion (148 ± 19 s) and a second occlusion on various LV function parameters were studied, as well as recovery of these parameters after reperfusion. Ischaemia caused an immediate (<5 s) decrease in diastolic function, followed by a decrease in contractile function, indicated by a rightward shift of the PV-loop, and a decreased dP/dtmax and ejection fraction. All parameters recovered within two minutes after reperfusion. The second occlusion caused a more rapid and more pronounced decrease in systolic and global LV function, while the 12-lead ECG showed less ST-segment deviation. CONCLUSIONS: Online LV pressure-volume measurements during elective PCI show that prolonged balloon coronary occlusion causes a phased ischaemic response of diastolic dysfunction, and then systolic dysfunction with more pronounced deterioration during a consecutive ischaemic period, paradoxical to the ischaemic electrocardiographic signs.

Effects of mechanical left ventricular unloading by Impella on left ventricular dynamics in high-risk and primary percutaneous coronary intervention patients.

OBJECTIVES: We studied online left ventricular (LV) dynamic effects of mechanical LV unloading directly after percutaneous coronary intervention (PCI). BACKGROUND: Limited clinical information is available on the direct LV dynamic consequences of LV unloading in patients undergoing high-risk PCI and primary PCI for acute ST-elevation myocardial infarction. METHODS: The effects of the Impella LP2.5 device on LV dynamics were studied in 11 patients (elective high-risk PCI, n = 6; primary PCI, n = 5). LV pressure and volume were continuously assessed by a pressure-conductance catheter at 4 different support levels of the Impella, from 0 L/min at baseline to 2.5 L/min at maximal support. RESULTS: The response to increased LV unloading was not different between both groups of patients. The pooled data showed no change on global and systolic LV function during increased LV unloading, while diastolic function showed improvement as indicated by an increased LV compliance in all patients. There was a decrease in end-diastolic pressure from 22 +/- 12 to 13 +/- 9 mm Hg (P = 0.0001), in end-diastolic elastance from 0.134 +/- 0.060 to 0.091 +/- 0.064 mm Hg/mL (P = 0.009), and in end-diastolic wall stress from 84 +/- 50 to 47 +/- 39 mm Hg (P = 0.004). CONCLUSIONS: LV unloading decreases end-diastolic wall stress and improves diastolic compliance dose-dependently. Our results indicate beneficial LV unloading effects of Impella during high-risk and primary PCI.

Acute left ventricular dynamic effects of primary percutaneous coronary intervention from occlusion to reperfusion.

OBJECTIVES: We studied the left ventricular (LV) dynamic effects of primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) by directly obtaining pressure-volume (PV) loops during the procedure. BACKGROUND: An acute myocardial infarction causes a decrease in LV compliance. The instantaneous effects of primary PCI on LV compliance are unknown. METHODS: We studied 15 consecutive patients (10 males, ages 59 +/- 12 years), who presented with their first acute anterior STEMI within 6 h after onset of symptoms, and in whom coronary angiography revealed an occluded left anterior descending coronary artery. Before performing primary PCI, we inserted a pressure-conductance catheter in the LV to continuously obtain PV loops. RESULTS: Immediately after successful reperfusion, significant improvements were observed in LV diastolic function, as indicated by an increased end-diastolic compliance with a 6.0 +/- 2.8 mm Hg (p < 0.0001) downward shift of the compliance curve. There was a decrease in end-diastolic pressure of 24 +/- 18% (p = 0.0002), in stiffness of 27 +/- 18% (p = 0.0003), and in wall stress of 20 +/- 24% (p = 0.004). Systolic function mainly showed an immediate improvement in apical contractility from 40 +/- 17% to 54 +/- 15% (p = 0.01). CONCLUSIONS: Primary PCI in anterior STEMI patients causes an immediate improvement in diastolic function, assessed by online PV loop measurements.

Effects of left ventricular unloading by Impella recover LP2.5 on coronary hemodynamics.

OBJECTIVES: We studied the effects of LV unloading by the Impella on coronary hemodynamics by simultaneously measuring intracoronary pressure and flow and the derived parameters fractional flow reserve (FFR), coronary flow velocity reserve (CFVR), and coronary microvascular resistance (MR). BACKGROUND: Patients with compromised left ventricular (LV) function undergoing high-risk percutaneous coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on coronary hemodynamics. METHODS: Eleven patients (mean LV ejection fraction of 35 +/- 11%) underwent PCI during LV support by the LV unloading device (Impella Recover LP2.5). Intracoronary measurements were performed in a nonstenotic coronary artery after the PCI, before and after adenosine-induced hyperemia at four different support levels (0-2.5 L/min). RESULTS: Aortic and coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 +/- 24 to 72 +/- 27 cm/sec, P = 0.001 and 1.88 +/- 0.52 to 2.34 +/- 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 +/- 1.32 to 1.89 +/- 1.43 mm Hg cm(-1) sec, P = 0.005). CONCLUSIONS: Unloading of the LV by the Impella increased aortic and intracoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella-induced increase in coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance.

Safety and feasibility of elective high-risk percutaneous coronary intervention procedures with left ventricular support of the Impella Recover LP 2.5.

Currently, the most used left ventricular (LV) support device is intra-aortic balloon counterpulsation. The percutaneous implantable Impella Recover LP 2.5 system is a novel LV (unloading) assist device. We studied the feasibility and safety of LV support with the percutaneous implantable Impella Recover LP 2.5 system in 19 consecutive high-risk patients with percutaneous coronary intervention. Procedural success using the device and percutaneous coronary intervention was achieved in all 19 patients, who were very poor candidates for surgery. The patients were elderly (84% were >60 years of age), 74% had previous myocardial infarction, 63% had LV ejection fractions of < or =25%, and all had LV ejection fractions of < or =40%. There were no procedural deaths and 2 device-unrelated in-hospital late deaths. Mean decrease in hemoglobin level was 0.7 +/- 0.4 mmol/L. The device did not induce or increase aortic valve regurgitation. There were no important device-related adverse events during LV support with the Impella Recover LP 2.5 system. However, these encouraging findings must be confirmed by larger studies, longer assist times, and in other patient categories.