Left Ventricular Systolic Volume Index Research Articles

Effects of Acute Triiodothyronine Treatment in Patients with Anterior Myocardial Infarction Undergoing Primary Angioplasty: Evidence from a Pilot Randomized Clinical Trial (ThyRepair Study).

Background: Thyroid hormone has a differential action on healthy and ischemic heart. Triiodothyronine (T3) administration improved postischemic cardiac function while it limited apoptosis in experimentally induced ischemia. Thus, the present study investigated the potential effects of acute liothyronine (LT3) treatment in patients with anterior myocardial infarction. Methods: This study is a pilot, randomized, double-blind, placebo-controlled trial (ThyRepair study). We randomized 52 patients and analyzed data from 37 patients (n = 16 placebo and n = 21 LT3), per prespecified per protocol analysis. We excluded three patients who had died of cardiovascular causes (one in placebo and two in LT3 arm), four with small infarct size below a pre-specified threshold (in the placebo arm), and the rest, who lacked follow-up data. LT3 treatment started after stenting as an intravenous (i.v.) bolus injection of 0.8 μg/kg of LT3 followed by a constant infusion of 0.113 μg/kg/h i.v. for 48 hours. All patients had cardiac magnetic resonance (CMR) at hospital discharge and 6 months follow-up. The primary end point was CMR left ventricular (LV) ejection fraction (LVEF) and secondary endpoints were LV volumes, infarct volume (IV), and safety. Results: The CMR LVEF% at 6 months was 53.6 ± 9.5 for the LT3-treated group and 48.6 ± 11 for placebo, p = 0.15. Acute LT3 treatment resulted in a significantly lower LV end-diastolic volume index (92.2 ± 16.8 mL/m2 vs. 107.5 ± 22.2, p = 0.022) and LV systolic volume index (47.5 ± 13.9 mL/m2 vs. 61.3 ± 21.7, p = 0.024) at hospital discharge, but not at 6 months. There was no statistically significant difference in CMR IV at hospital discharge between the groups (p = 0.24). CMR IV tended to be lower in the LT3-treated group at 6 months (18.7 ± 9.5 vs. 25.9 ± 11.7, in placebo, p = 0.05). Serious, life-threatening events related to LT3 treatment were not observed. A tendency for an increased incidence of atrial fibrillation (AF) was found in the LT3 group during the first 48 hours (19% for T3 group vs. 5% for placebo, p = 0.13). Conclusion: This pilot randomized, placebo-controlled trial study suggests potential favorable effects (acute cardiac dilatation and 6-month IV) as well as potential concerns regarding a higher risk of AF after LT3 administration early after myocardial infarction, which should be tested in a larger scale study.

Myocardial tissue function and characterization in patients with idiopathic cardiac magnetic resonance myopericarditis: evolutionary analysis

Abstract Introduction The identification of prognostic markers related to the occurrence of events and recovery of ventricular function may be important in patients with acute myopericarditis (AMP). There is still a lack of data related to tissue characterization by cardiac magnetic resonance (CMR) of AMP, evolution and definition of possible long-term prognostic markers. Purpose To evaluate the myocardial tissue characterization of CMR related to the occurrence of combined events (death from all causes, heart failure and AMP recurrence) and the increase in left ventricular ejection fraction (LVEF) in patients with AMP. Methods Inclusion criteria were chest pain and/or electrocardiographic changes associated with elevated troponin (above the 99th percentile) in the absence of coronary stenosis and diagnosis of AMP by CMR <48 hours of admission confirmed by the presence of edema and/or late enhancement. After a follow-up of up to 24 months, 100 patients remained and in the assessment of the increase in LVEF (increase >5%), 36 cases remained, recalled for a new CMR between 6 and 18 months from the initial event. Results Significant differences in CMR were found between patients who had combined events (n=26) versus no combined events (n=74) in the following characteristics evaluated: initial LVEF (OR=0.938; CI: 0.895–0.984, p=0.008), left ventricular (LV) systolic volume index (OR=1.034; CI: 1.005–1.062, p=0.019), LV diastolic volume index (OR=1.029; CI: 1.002–1.056, p=0.038), presence of hypersignal in T2 (OR=11.325; CI: 2.247–57.075, p=0.003), presence of late anteroseptal enhancement (OR=0.160; CI: 0.037–0.685, p=0.014), basal anteroseptal (OR=0.255; CI: 0.071–0.914, p=0.036) and lateral apical (OR=5.902; CI: 1.236–28.187, p=0.026). In relation to the increase in LVEF, significant differences were found in CMR in the following characteristics evaluated: LVEF (OR=0.870; CI: 0.758–0.988, p=0.047), end systolic volume of the right ventricle (OR=1.047; CI: 1.001–1.096, p=0.047), LV systolic diameter (OR=1.283; CI: 1.034–1.593, p=0.023), LV diastolic diameter (OR=1.225; CI: 1.012–1.482, p=0.038), LV systolic volume index (OR=1.340; CI: 1.066–1.685, p=0.012), LV diastolic volume index (OR=1.111; CI: 1.017–1.213, p=0.019) and right ventricular systolic volume index (OR=1.116; CI: 1.006–1.236, p=0.037). Conclusion We observed a significant association between combined events in the long-term follow-up with initial LVEF, LV systolic and diastolic volume indexes, T2 hypersignal and the presence of mid and basal anteroseptal and lateral apical late enhancement. Already related to the increase in LVEF in evolutionary CMR, we observed a significant association with initial LVEF, end systolic volume of the right ventricle, LV systolic and diastolic diameters, LV systolic and diastolic volume indexes and right ventricle systolic volume index. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): FAPESP

Impact of Intubation Time on Survival following Coronary Artery Bypass Grafting: Insights from the Surgical Treatment for Ischemic Heart Failure (STICH) Trial

The authors aimed to assess determinants of intubation time and evaluate its impact on 30-day and 1-year postoperative survival in Surgical Treatment for Ischemic Heart Failure (STICH) trial patients. A multivariable Cox proportional hazards model was used among the 1,446 surgical patients from the STICH trial who survived 36 hours after operation, in order to identify perioperative factors associated with 30-day and 1-year postoperative mortality. A multivariable logistic regression model was used to determine risk factors associated with intubation time. At 36 hours post-operation, 1,298 (out of 1,446) were extubated and 148 (10.2%) still intubated. Median postoperative intubation time was 11.4 hours. Among patients surviving 36 hours, a multivariable model was developed to predict 30-day (c-index = 0.88) and 1-year (c-index = 0.78) mortality. Intubation time was the strongest independent predictor of 30-day (hazard ratio [HR] 5.50) and 1-year mortality (HR 3.69). Predictors of intubation time >36 hours included mitral valve procedure, New York Heart Association class, left ventricular systolic volume index, creatinine, previous coronary artery bypass grafting (CABG), and age. Results were similar in patients surviving 24 hours post-operation, where intubation time was also the strongest predictor of 30-day (HR 4.18, c-index 0.87) and 1-year (HR 2.81, c-index 0.78) mortality. Intubation time is the strongest predictor of 30-day and 1-year mortality among patients with ischemic heart failure undergoing CABG. Combining intubation time with other mortality risk factors may allow the identification of patients at the highest risk for whom the development of specific strategies may improve outcomes.

Left ventricular remodelling in systolic heart failure using ivabradine. Slower is smaller is better?

This editorial refers to ‘Effects of selective heart rate reduction with ivabradine on left ventricular remodelling and function: results from the SHIFT echocardiographic substudy’ by J.C. Tardif et al. , doi:10.1093/eurheartj/ehr311 Tardif and co-workers have published the echocardiographic substudy of the SHIFT trial.1 This pre-defined substudy included 611 out of 6505 patients from SHIFT, or, in other words, 9.3% of the entire cohort studied in SHIFT.2 The authors report that of these 611 patients, 96 ivabradine- and 104 placebo-treated patients had to be excluded, mainly due to incomplete or unreadable echo recordings, which left 208 patients in the ivabradine group and 203 in the placebo group for analysis. The echoes were analysed centrally and the investigations were done at baseline and after 8 months, with the primary endpoint of change of left ventricular systolic volume index (LVESVI) at 8 months. This well-treated population [92% were on beta-blockers, with 56% taking 50% of the recommended dose, and 94% were treated with a renin–angiotensin system (RAS) antagonist] was not different from the entire SHIFT cohort, except for a lower rate of hypertension and a …

Characterization of the Peri-Infarct Zone by Contrast-Enhanced Cardiac Magnetic Resonance Imaging Is a Powerful Predictor of Post–Myocardial Infarction Mortality

Accurate risk stratification is crucial for effective treatment planning after myocardial infarction (MI). Previous studies suggest that the peri-infarct border zone may be an important arrhythmogenic substrate. In this pilot study, we tested the hypothesis that the extent of the peri-infarct zone quantified by contrast-enhanced cardiac magnetic resonance (CMR) is an independent predictor of post-MI mortality. We studied 144 patients with documented coronary artery disease and abnormal myocardial delayed enhancement (MDE) consistent with MI. A computer-assisted, semiautomatic algorithm quantified the total infarct size and divided it into the core and peri-infarct regions based on signal-intensity thresholds (>3 SDs and 2 to 3 SDs above remote normal myocardium, respectively). The peri-infarct zone was normalized as a percentage of the total infarct size (%MDE(periphery)). After a median follow-up of 2.4 years, 29 (20%) patients died. Patients with an above-median %MDE(periphery) were at higher risk for death compared with those with a below-median %MDE(periphery) (28% versus 13%, log-rank P<0.01). Multivariable analysis showed that left ventricular systolic volume index and %MDE(periphery) were the strongest predictors of all-cause mortality (adjusted hazard ratio [HR] for %MDE(periphery), 1.45 per 10% increase; P=0.002) and cardiovascular mortality (adjusted HR, 1.51 per 10% increase; P=0.009). Similarly, after adjusting for age and left ventricular ejection fraction, %MDE(periphery) maintained strong and independent associations with all-cause mortality (adjusted HR, 1.42; P=0.005) and cardiovascular mortality (adjusted HR, 1.49; P=0.01). In patients with a prior MI, the extent of the peri-infarct zone characterized by CMR provides incremental prognostic value beyond left ventricular systolic volume index or ejection fraction. Infarct characteristics by CMR may prove to be a unique and valuable noninvasive predictor of post-MI mortality.

Technique and outcome of mitral valve replacement in dogs

Eight dogs with naturally occurring severe mitral regurgitation underwent mitral valve replacement with a mechanical valve prosthesis during cardiopulmonary bypass. Dogs received warfarin orally after surgery to maintain a prothrombin time-based international normalized ratio from 2.5 to 3.5. Seven dogs survived surgery. Left ventricular diastolic volume index decreased significantly from 206 +/- 91 mL/m2 before surgery to 121 +/- 47 mL/m2 after surgery. Left atrium-to-aorta ratio decreased significantly from 2.66 +/- 0.4 before surgery to 1.73 +/- 0.65 after surgery. Left ventricular systolic volume index was not significantly different after surgery (56 +/- 36 mL/m2), compared with before surgery (40 +/- 32 mL/m2). Median survival after surgery was 4.5 months (range, 0.75 months to 5.25 years). Six dogs died of confirmed or suspected thrombosis of the valve prosthesis. Dogs with severe mitral regurgitation tolerated mitral valve replacement well, but a high incidence of prosthetic valve thrombosis limited long-term outcome.

Right ventricular function in patients with acute anterior myocardial infarction: tissue Doppler echocardiographic approach

Objective — Our purpose was to investigate the right ventricular (RV) performance of patients with a first acute anterior myocardial infarction (AAMI) by using pulsed wave Doppler tissue (PWDT) samplings of tricuspid annulus and RV free wall.Methods and results — The study group included 31 patients with AAMI and 20 age-matched controls. Conventional indexes of RV functions were the magnitude of tricuspid annular plane systolic excursion (TAPSE), and the transpulmonary and transtricuspid Doppler parameters. PWDT velocities were obtained by placing the sample volume at the lateral tricuspid annulus and the mid-segment of RV free wall; the peak systolic (S), early (E) and late (A) diastolic PWDT velocities and time intervals from ECG-Q wave to their peaks were analysed. Standard indexes were comparable except TAPSE that was significantly lower in AAMI-patients (p < 0.001). S velocities were similar; A of both regions (p = 0.018 and 0.012) and E of RV free wall (p = 0.011) were significantly increased in AAMI-group. Q-Sa intervals in both regions (p = 0.007 and 0.015) and Q-Ea of tricuspid annulus (p = 0.045) were significantly shorter in patients with AAMI.TAPSE and E of RV free wall had significant negative correlations with left ventricular systolic volume index and right atrial filling fraction (AFF), respectively (r = -0.46, p = 0.01 for both). A of tricuspid annulus had a positive correlation with left AFF (r = 0.42, p = 0.02).Conclusion — PWDT imaging of tricuspid annulus and RV free wall is capable to sensitively detect the adaptive mechanisms and unfavourable diastolic properties of RV dynamics in patients with AAMI.

Effects of captopril on left ventricular systolic and diastolic function after acute myocardial infarction

The left ventricle progressively dilates in some patients after acute myocardial infarction (AMI). Both systolic and diastolk left ventricular (LV) dysfunction can be of significance in the development of heart failure. Captopril has been shown to prevent dilatation, but the effect on LV diastolic function is unknown. In a placebo-controlled double-blind parallel study, 58 AMI patients with heart failure or low ejection fraction, or both, were consecutively randomized at day 7 to either placebo or captopril (25 mg twice daily). No differences were present between the groups at baseline. Fifty-three patients completed the 6-month study period. Both LV diastolic and systolic volume indexes increased significantly in the placebo group (17 and 14%, respectively); in the captopril group there was no change in LV diastolic volume index, but a 13% reduction in LV systolic volume index. Ejection fraction increased significantly in the captopril group. The peak flow velocities of the early and atrial filling phases were measured, and the ratio between the velocities was calculated. A significant reduction was observed during the study period in early peak flow velocity (65 to 52 cm/s) and in the ratio between early and atrial peak flow velocity (1.3 to 0.8) in the placebo group (p < 0.05), but no significant changes occurred in the captopril group. No correlation was found between dilatation of the left ventricle and reduction in early peak flow velocity or the ratio between early and atrial peak flow velocity. In conclusion, captopril prevented LV dilatation, improved ejection fraction and prevented LV diastolic dysfunction in AMI patients with early signs of LV systolic dysfunction.

Effects of intravenous administration of nicorandil on cardiovascular hemodynamics and left ventricular function

The effects of the intravenous administration of the antianginal drug, nicorandil, 50 μg/kg administered over 2 minutes, were investigated during pacing-induced ischemia in 8 patients with coronary artery disease. Hemodynamic parameters were measured and single-plane left ventriculograms were obtained in control and postpacing periods both before and after pretreatment with nicorandil. Regional wall motion of the left ventricle was assessed by measuring shortening of the radial axes originating from the center of gravity of the end-diastolic silhouette. Heart rate, left ventricular (LV) systolic pressure and end-diastolic volume index did not change in the immediate postpacing period with or without medication. LV end-diastolic pressure decreased with nicorandil, from 22.0 ± 3.4 to 17.0 ± 2.3 mm Hg (mean ± standard error of the mean) (p < 0.05), and LV systolic volume index, from 39.6 ± 8.0 to 30.4 ± 6.8 ml/m 2 (p < 0.05). Ejection fraction increased from 55.2 ± 5.0 to 64.3 ± 3.8% (p < 0.05). Stroke index and cardiac index (calculated from heart rate and stroke index) did not change significantly. Rapid right ventricular pacing increased the extent and degree of dyskinesia of the left ventricle, but premedication with nicorandil improved the wall motion. Thus, nicorandil has salutary effects on ventricular contractile and hemodynamic responses to transient ischemia induced by pacing stress.

Relationship of cardiac chamber volume to baroreflex activity in normal humans.

The objectives of this study were to examine the effect of incremental lower body negative pressure (LBNP) on cardiac chamber volume and assess the relationship between cardiac chamber volume and baroreflex activation of the neurohormonal axis. Accordingly, echocardiographic determination of cardiac chamber volume and neurohormonal responses were studied in 14 normal subjects during incremental LBNP. LBNP -10 mm Hg decreased left atrial diameter and left ventricular systolic volume index, but did not alter heart rate, systolic or pulse pressure, or stroke volume. During LBNP -10 mm Hg, plasma norepinephrine levels increased, suggesting activation of the sympathetic nervous system. LBNP -40 mm Hg caused a significant decrease in left atrial diameter and left ventricular systolic, diastolic, and stroke volume indices. During LBNP -40 mm Hg, heart rate increased, and systolic and pulse pressure fell. With this more negative level of LBNP, norepinephrine, angiotensin II, aldosterone, and arginine vasopressin concentrations and PRA all increased. The findings that left atrial diameter decreased and plasma norepinephrine concentration increased during LBNP -10 mm Hg suggest that the sympathetic nervous system is sensitive to changes in atrial receptor activity. At higher levels of LBNP (-40 mm Hg), activation of the renin-angiotensin system and release of vasopressin were associated with a fall in left ventricular diastolic volume as well as a decrease in the pressure input to the arterial baroreceptors. Under this condition, the differential contribution of the cardiopulmonary and arterial baroreceptors to the regulation of the renin-angiotensin system and vasopressin release cannot be distinguished.

Beneficial Effects of Nicorandil on Cardiovascular Hemodynamics and Left Ventricular Function

The effects of sublingual nicorandil (5 mg), an antianginal drug, were investigated in pacing-induced ischemia in 11 patients with coronary artery disease. Hemodynamic parameters were measured, and single-plane left ventriculograms were obtained in control and postpacing periods both before and after pretreatment with nicorandil. Regional wall motion of the left ventricle was assessed by measuring shortening of the radial axes originating from the center of the gravity of the end-diastolic silhouette. Heart rate, left ventricular (LV) systolic pressure, and end-diastolic volume index were not changed in immediate postpacing with or without medication. The LV end-diastolic pressure decreased from 22.0 +/- 1.8 (SEM) to 18.4 +/- 1.7 mm Hg (p less than 0.01) and LV systolic volume index from 48.5 +/- 7.1 to 37.4 +/- 7.7 ml/m2 (p less than 0.01). Ejection fraction increased from 42.2 +/- 3.7 to 56.7 +/- 3.7% (p less than 0.01), stroke index (SI) from 34.5 +/- 3.7 to 43.1 +/- 2.2 ml/beat/m2 (p less than 0.01), and cardiac index (calculated from heart rate and SI) from 2.49 +/- 0.30 to 3.09 +/- 0.19 L/min/m2 (p less than 0.01). With rapid right ventricular pacing, dyskinesis of the left ventricle increased in both area and degree, but was improved with premedication with nicorandil. Thus, nicorandil has salutary effects on ventricular contractile and hemodynamic responses to transient ischemia induced by pacing stress.