Changes In Left Ventricular Mechanics Research Articles

Left ventricular mechanics during right ventricular apical or left ventricular-based pacing in patients with chronic atrial fibrillation after atrioventricular junction ablation

ObjectivesThe aim of the study was to evaluate whether left ventricular (LV) mechanics are better under LV-based pacing than under right ventricular (RV) apical pacing in patients with permanent atrial fibrillation (AF) after atrioventricular junction (AVJ) ablation. Background“Ablate and pace” is an acceptable therapy for drug-refractory AF. However, the RV apical stimulation commonly used seems to interfere with the beneficial hemodynamic effect of regularization of heart rhythm. MethodsThe study included 12 patients (5 men, mean age 62 ± 8.3 years), 6 with impaired and 6 with normal LV systolic function. All of them had a biventricular pacemaker system implanted and underwent atrioventricular node ablation for drug-refractory chronic AF. Using a conductance catheter, we analyzed LV pressure–volume loops during routine coronary angiography in order to evaluate short-term changes in LV mechanics during RV apical and LV-based (LV free wall or biventricular) pacing. ResultsCompared with RV pacing, LV-based pacing significantly improved the indexes of LV systolic function (i.e., end-systolic pressure and volume, cardiac index, stroke work, preload recruitable stroke work, maximal rate of rise of LV pressure [dP/dtmax], LV ejection fraction, and end-systolic elastance). The LV diastolic filling indexes, end-diastolic pressure and volume, were better during LV-based pacing, whereas LV diastolic function indexes, −dP/dtmax, passive diastolic chamber stiffness, and time constant of LV isovolumic relaxation showed no clear change. ConclusionsIn the short term, LV-based pacing is superior to RV apical pacing in terms of contractile function and LV filling after AVJ ablation for drug-refractory AF.

Left Ventricular Mechanics and Myocardial Blood Flow Following Restoration of Normal Activation Sequence in Paced Patients With Long-term Right Ventricular Apical Stimulation

Asynchronous ventricular activation, as induced by ventricular pacing, is known to affect left ventricular (LV) systolic and diastolic function and myocardial blood flow. However, it is not clear whether the long-term disturbances it causes are reversible after the restoration of the normal ventricular activation sequence. In this study, we used the conductance catheter method and a Doppler guidewire to assess the changes in LV mechanics, and correspondingly in myocardial blood flow, after the restoration of the normal ventricular activation sequence in patients with long-term right ventricular apical pacing. Sixteen patients (mean [+/- SD] age, 61 +/- 11 years; 9 men) with right ventricular apical stimulation and complete ventricular pacing capture for a very long period were studied. In eight patients, we analyzed pressure-volume loops before and immediately after the restoration of the normal ventricular activation sequence, and in the remaining eight patients the myocardial blood flow and flow reserve were analyzed. End-systolic elastance (Ees) [5.503 +/- 0.6 vs 4.287 +/- 0.28 mm Hg/mL, respectively; p = 0.003] and its ratio to effective arterial elastance (1.63 +/- 0.51 vs 2.00 +/- 0.64, respectively; p = 0.009), which are indexes of systolic function and ventriculoarterial coupling, respectively, improved significantly after restoration of the normal ventricular activation sequence. Indexes of diastolic function and the predicted myocardial oxygen consumption (MO(2)) showed no clear change. Coronary flow in the dominant coronary artery increased significantly (46.55 +/- 14.12 vs 71.55 +/- 27.53 mL/min, respectively; p = 0.002), while the coronary flow reserve in the same artery decreased (3.5 +/- 1.0 vs 2.6 +/- 0.5, respectively; p = 0.008). The restoration of a normal activation sequence after long-term ventricular asynchrony enhances acutely contractile function without affecting MO(2). These changes in LV function do not appear to have causal relationships with myocardial blood flow changes.

727-2 Changes in Left Ventricular Mechanics and Energetics in Canine Microembolization Model of Heart Failure

Myocardial mechanics and energetics have been shown previously to be markedly abnormal in a canine model of pacing induced heart failure. However, whether those abnormalities pertain to other, more clinically relevant forms of heart failure is unknown. To investigate this question, heart failure was created by ischemic damage in 6 dogs (CHF group) that underwent repeated coronary microsphere injections over 2 months resulting in afinal area ejection fraction (aEF) of 34 ± 4%. A control group of 6 normal dogs had an aEF of 46 ± 8%, Hearts of these animals were isolated, cross-perfused and balloons placed in the LV to control volume. We measured the LV endsystolic (ESPVR) and end-diastolic (EDPVR) pressure-volume relations and the relationship between oxygen consumption (mVO 2 ) and pressure-volume area (PVA). β-responsiveness of the CHF group was significantly depressed compared to control as assessed by the increased amount of isoproterenol required to increase peak isovolumic LV pressure by 40% (72 ± 36 vs. 29 ± 14 pg/min, p < 0.05) providing pharmacologic evidence of the heart failure state, CHF hearts had a depressed and dilated LV as assessed by the ESPVR slope, Ees, and volume axis intercept, Vo, (both normalized to LV mass) compared to control (TABLE). EDPVR of CHF hearts was shifted to the right compared to control. Systolic and diastolic stress-strain relationships. estimated from the pressure-volume relations. were similar in the two groups. These data suggest that with the degree of chronic ischemic damage achieved, there was systolic LV chamber dysfunction and chamber remodeling but not myocardial property changes in surviving muscle. The mVO 2 -PVA relation in CHF hearts had smaller mVO 2 -intercept (B) than control with no change in the slope (A) (TABLE). This contrasts with a previous report using a rapid pacing CHF model in which myocardial strength was decreased, A was decreased and B was unchanged. These data suggest that 1) in spite of the notable structural and functional changes in chamber mechanics, energetic aspects of the failing heart remained unaltered in this model and 2) conclusions about myocardial energetics in CHF are model dependent. ESPVR: Ees mmHg/ml.l00 g Vo ml/l00 g mVO 2 -PVA: A mlO 2 /mmHg/ml B mlO 2 /beat/l00 g CHF 3.9 ± 1.2 * 6.9 ± 5.3 ** (1.3 ± 04) × 10 -5 0.030 ± 0.005 ** Control 47 ± 1.9 0.5 ± 2.9 (1.3 ± 0.6) × 10 -5 0.036 ± 0.004 * p < 0.05. ** p < 0.01 vs. Control by ANCOVA

Transient changes in left ventricular mechanics during attacks of Prinzmetal angina: A two-dimensional echocardiographic study

Fifty-five ischemic attacks at rest with ST segment elevation were recorded by two-dimensional echocardiography (2DE) in 20 patients with Prinzmetal angina. Eighteen ischemic attacks were recorded starting from intravenous injection of ergonovine maleate while 37 spontaneous ischemic attacks were recorded from onset of either anginal pain or ECG changes or from the basal state. In each ischemic attack at least one of the following transient alterations was observed by 2DE during ST elevation: (1) Regional hypokinesia, akinesia, or dyskinesia; (2) “step sign,” that is, a sharp demarcation between an akinetic or dyskinetic area and an adjacent normal or hypercontracting region; and (3) geometric changes in left ventricular shape, that is, globular appearance in diastole and hourglass silhouette in systole. Regional myocardial asynergy was detected earlier than onset of pain (which was not present in 21 [38%] ischemic episodes) or ST segment elevation on ECG, as documented in 40 ischemic episodes (16 induced and 24 spontaneous) in which echocardiographic monitoring was performed from basal state and carried on up to the appearance of ischemia. All described mechanical changes were fully reversible after pain subsided and ST segment was back to isoelectric, either spontaneously or with nitrates; furthermore, a contractile “rebound phenomenon” of the previously ischemic wall was observed in some episodes. In conclusion, these results outline a role for 2DE in detecting cardiac mechanical impairment due to transient myocardial ischemia with ST segment elevation in humans.

Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: An M-mode echocardiographic study

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (−76.3 ± 9.1%) (mean ± SEM), in diastolic thickness (−11.7 ± 2.5%), and in percent systolic thickening (−88.0 ± 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 ± 2.1%) and decrease in percent fractional shortening (−38.1 ± 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.

Myocardial oxygen consumption in left ventricular hypertrophy and its relation to left ventricular mechanics

Alterations in left ventricular (LV) mechanics have significant effects on myocardial oxygen consumption (MV̇O 2 2) as a result of changing LV pressure and dimensions. However, the effects of load alteration on MV̇O 2 2 in the setting of LV hypertrophy and LV dysfunction have not been well characterized. Therefore, we examined changes in LV mechanics and MV̇O 2 2 in 32 patients with varying degrees of LV hypertrophy and LV dysfunction before and after pharmacologic alteration of load. With phenylephrine or nitroglycerin-induced load alteration, changes in peak systolic meridional stress, mean systolic stress and the area of a stress-dimension loop all correlated modestly with changes in MV̇O 2 2 (r = 0.66, 0.62, 0.63, respectively). However, changes in the time integral of LV ejection stress, or shortening load, were significantly correlated with changes in MV̇O 2 2 (r = 0.88, p < 0.001). In particular, load reduction results in a beneficial effect on MV̇O 2 2. In addition, for a given change in LV systolic pressure, changes in shortening load (38 + 3.7%) were significantly greater than changes in tension-time index (13 ± 1.4%), thus providing a sensitive marker of alteration of mechanical load. We conclude that physiologic alterations in mechanical load in normal persons as well as patients with LV hypertrophy are reflected in significant changes in the time integral of LV ejection stress. These changes in shortening load, mediated by changing LV pressure and dimension, are significantly related to changes in MV̇O 2 2.