Impact Of Left Ventricular Hypertrophy Research Articles

Determinant and Impact of Left Ventricular Hypertrophy (LVH) in Chronic Renal Failure (CRF) Patients

Left ventricular hypertrophy is the most common cardiovascular complication in chronic renal failure. It appears to be associated with excess mortality. Objective: To determine the factors associated with left ventricular hypertrophy (LVH) in patients with chronic kidney disease (CKD), and to describe their influence on renal function. Patients and methods: This was a descriptive and analytical study conducted over 6 years (January 1, 2012 to December 31, 2017) on CKD patients who had an electrocardiogram or cardiac ultrasound. Results: A total of 329 patients were included. LVH was found in 223 patients, a prevalence of 68%. The sex ratio M/F was 2.1. Mean age was 51.05±14.17 years (range 11-95 years). Arterial hypertension predominated (97% of cases), followed by diabetes (26%).Univariate and multivariate analysis showed that LVH was associated with: age ≤51 years (p=0.0037) and with arterial hypertension (p=0.0018) and anemia (p=0.0018). Over a 5-year period, CKD patients with LVH experienced a more rapid decline in renal function than those without LVH (p<0.0001). There was also a higher rate of death in patients with LVH (83%) than in those without (46%) during a 5-year follow-up. Conclusion: LVH is an important factor in the poor prognosis of CKD. This calls for systematic screening and early management by a multidisciplinary team.

Impact of left ventricular hypertrophy on frequency and complexity of ventricular arrhythmia among hypertensive Egyptian patients

BackgroundLeft ventricular hypertrophy (LVH) is associated with an increased risk of ventricular arrhythmias and cardiovascular mortality. The study objective was to investigate the effect of LVH severity on the complexity and severity of ventricular arrhythmias among a subset of Egyptian hypertensive patients.ResultsThe study cohort consisted of 60 hypertensive patients with LVH as diagnosed by echocardiography. Their mean age was (53.7 ± 12.3) years. 36 males (40%) and 24 females (60%). Diabetes mellitus was found in 26 patients (43%), 41% of these cases were smokers. 48-h Holter monitoring was performed in all cases to assess the frequency of ventricular premature contractions (VPC) and their complexity using the Lown grading. Increasing posterior wall thickness end diastole (PWTd) was an independent predictor of increasing VPC frequency, each 1 mm increase in the PWTd is associated with a 1.26% increase in the VPC% among total heart beats (b = 12.6, p < 0.001). Higher-grade VPCs—defined as grade 4a, 4b, and 5—were seen in 29 patients (48.3%). Interventricular septum thickness end diastole, PWTd, left ventricular mass, and left ventricular mass index (LVMI), were significantly higher among patients with higher Lown grading (p < 0.001). Using logistic regression analysis, female sex and LVMI were independent predictors of more complex VPC (OR = 8.766, p = .014), (OR = 1.096, p < 0.001), respectively. Among females, LVMI of more than 120 g/m2 can differentiate between high- and low-grade VPCs with 71% sensitivity and 80% specificity, while among males, LVMI of more than 129.5 g/m2 can differentiate between high and low-grade VPCs with 86% sensitivity and 66% specificity.ConclusionsThe frequency and complexity of ventricular arrhythmias among hypertensive heart disease are correlated with the severity of ventricular hypertrophy. Female sex and increasing left ventricular mass index are independent predictors of more complex forms of ventricular arrhythmias.

Determinant and Impact of Left Ventricular Hypertrophy (LVH) in Chronic Renal Failure (CRF) Patients

Left ventricular hypertrophy is the most common cardiovascular complication in chronic renal failure. It appears to be associated with excess mortality. Objective: To determine the factors associated with left ventricular hypertrophy (LVH) in patients with chronic kidney disease (CKD), and to describe their influence on renal function. Patients and methods: This was a descriptive and analytical study conducted over 6 years (January 1, 2012 to December 31, 2017) on CKD patients who had an electrocardiogram or cardiac ultrasound. Results: A total of 329 patients were included. LVH was found in 223 patients, a prevalence of 68%. The sex ratio M/F was 2.1. Mean age was 51.05±14.17 years (range 11-95 years). Arterial hypertension predominated (97% of cases), followed by diabetes (26%).Univariate and multivariate analysis showed that LVH was associated with: age ≤51 years (p=0.0037) and with arterial hypertension (p=0.0018) and anemia (p=0.0018). Over a 5-year period, CKD patients with LVH experienced a more rapid decline in renal function than those without LVH (p&lt;0.0001). There was also a higher rate of death in patients with LVH (83%) than in those without (46%) during a 5-year follow-up. Conclusion: LVH is an important factor in the poor prognosis of CKD. This calls for systematic screening and early management by a multidisciplinary team.

Left atrial mechanics evaluated by two-dimensional strain analysis: alterations in essential hypertension.

Hypertension is a cardiovascular risk factor that predisposes to cardiac structural alterations namely increased left ventricular (LV) wall thickness, reduced LV compliance and diastolic dysfunction, with consequent left atrial (LA) dilation and functional impairment. In this article, we evaluated differences in left atrial structure and function using two-dimensional speckle tracking echocardiography in patients with hypertension compared with controls. This was a retrospective cross-sectional study of 208 hypertensive patients and 157 controls who underwent a comprehensive transthoracic echocardiogram. Patients with hypertension were stratified by the presence of left ventricular hypertrophy (LVH). Non-LVH hypertension patients had lower left atrial reservoir strain (LAS RES ) (34.78 ± 29.78 vs. 29.78 ± 6.08; P = 0.022) and conduit strain (LAS CD ) (19.66 ± 7.29 vs. 14.23 ± 4.59; P = 0.014) vs. controls despite similar left atrial volumes (LAV) . Left atrial contractile strain (LAS CT ) was not significantly different between non-LVH hypertension patients and controls (15.12 ± 3.77 vs. 15.56 ± 3.79; P = 0.601). Left atrial mechanical dispersion was significantly higher in the LVH group compared with the non-LVH hypertension group (42.26 ± 13.01 vs. 50.06 ± 14.95; P = 0.009). In multivariate regression analysis, LVH correlated with left atrial mechanical dispersion ( P = 0.016). An age-hypertension interaction independently correlated with LAS CT ( P < 0.001). Hypertension results in functional left atrial changes even before development of LV hypertrophy and structural left atrial changes with increased left atrial volume. We demonstrate both a likely hypertension-associated left atrial myopathy that prevents age-related compensatory increase in left atrial contractile function, and impact of LVH in hypertension on left atrial dyssynchrony.

Impact of left ventricular hypertrophy on clinical outcomes in patients with dialysis: a single-center study in Japan.

Left ventricular hypertrophy (LVH) is a well-known risk factor for poor clinical outcomes in patients undergoing dialysis. However, little evidence supports the above notion in Japan, and the influence of subtypes of LVH on prognosis. We investigated 367 patients undergoing dialysis who underwent routine echocardiographic examinations between April and September 2018. LVH was defined as any LV mass ≥ 115g/m2 in men and ≥ 95g/m2 in women obtained by echocardiography. The primary endpoint was a composite outcome including all-cause death, admission due to heart failure, and ischemic heart event or stroke. LVH was divided into subtype-groups according to eccentric hypertrophy or concentric hypertrophy, and with and without hypertension. LVH was observed in 171 (47%) patients. The primary endpoint was observed in 58 patients (16%) during the median follow-up period of 500days. Multivariable Cox regression analyses identified four independent risk factors for the primary endpoint: age, pulse rate, serum albumin level, and LV mass index (per 10-g/m2 increase; hazard ratio: 1.12, 95% confidence interval: 1.06-1.18, P < 0.001). Kaplan-Meier analyses demonstrated that patients with LVH had a worse prognosis than those without LVH in terms of the primary endpoint (log-rank P < 0.001). The incidence of the primary outcome was not significantly different between patients with eccentric or concentric hypertrophy, and between LVH patients with and without hypertension. Japanese patients with LVH undergoing dialysis had a worse prognosis than those without LVH in terms of the composite clinical endpoint.

Left Ventricular Hypertrophy Increases Susceptibility to Bupivacaine-induced Cardiotoxicity through Overexpression of Transient Receptor Potential Canonical Channels in Rats.

Local anesthetics, particularly potent long acting ones such as bupivacaine, can cause cardiotoxicity by inhibiting sodium ion channels; however, the impact of left ventricular hypertrophy on the cardiotoxicity and the underlying mechanisms remain undetermined. Transient receptor potential canonical (TRPC) channels are upregulated in left ventricular hypertrophy. Some transient receptor potential channel subtypes have been reported to pass relatively large cations, including protonated local anesthetics; this is known as the "pore phenomenon." The authors hypothesized that bupivacaine-induced cardiotoxicity is more severe in left ventricular hypertrophy due to upregulated TRPC channels. The authors used a modified transverse aortic constriction model as a left ventricular hypertrophy. Cardiotoxicity caused by bupivacaine was compared between sham and aortic constriction male rats, and the underlying mechanisms were investigated by recording sodium ion channel currents and immunocytochemistry of TRPC protein in cardiomyocytes. The time to cardiac arrest by bupivacaine was shorter in aortic constriction rats (n =11) than in sham rats (n = 12) (mean ± SD, 1,302 ± 324 s vs. 1,034 ± 211 s; P = 0.030), regardless of its lower plasma concentration. The half-maximal inhibitory concentrations of bupivacaine toward sodium ion currents were 4.5 and 4.3 μM, which decreased to 3.9 and 2.6 μM in sham and aortic constriction rats, respectively, upon coapplication of 1-oleoyl-2-acetyl-sn-glycerol, a TRPC3 channel activator. In both groups, sodium ion currents were unaffected by QX-314, a positively charged lidocaine derivative, that hardly permeates the cell membrane, but was significantly decreased with QX-314 and 1-oleoyl-2-acetyl-sn-glycerol coapplication (sham: 79 ± 10% of control; P = 0.004; aortic constriction: 47± 27% of control; P = 0.020; n = 5 cells per group). Effects of 1-oleoyl-2-acetyl-sn-glycerol were antagonized by a specific TRPC3 channel inhibitor. Left ventricular hypertrophy exacerbated bupivacaine-induced cardiotoxicity, which could be a consequence of the "pore phenomenon" of TRPC3 channels upregulated in left ventricular hypertrophy.

THE IMPACT OF LEFT VENTRICULAR HYPERTROPHY ON OPTIMAL BLOOD PRESSURE CONTROL

Objective:We aimed to investigate the determinant factors of blood pressure (BP) control achievement and in particular the impact of left ventricular hypertrophy (LVH) regression, determined by echocardiography, in hypertensive patients during a follow up period under treatment.Design and method:238

Impact of left ventricular hypertrophy on long-term clinical outcomes in hypertensive patients who underwent successful percutaneous coronary intervention with drug-eluting stents.

Left ventricular hypertrophy (LVH) is associated with increased risk for vascular events and mortality. This study investigated 8-year clinical outcomes of hypertensive patients with LVH who underwent percutaneous coronary intervention (PCI) with drug-eluting stents (DES) compared with hypertensive patients without LVH.A total of 1704 consecutive hypertensive patients who underwent PCI from 2004 to 2014 were enrolled. We classified them into either the LVH group (n = 406) or the control group (without LVH, n = 1298). LVH was defined by LV mass index > 115 g/m2 in men and > 95 g/m2 in women. After propensity score matched (PSM) analysis, 2 PSM groups (366 pairs, n = 732, c-statistic = 0.629) were generated.For up to 8 years, the LVH group showed a higher incidence of cardiac death (4.4% vs 1.2%, log-rank P = .023, hazard ratio: 3.371, 95% confidence interval: 1.109–10.25; P = .032) compared with the control group. However, there were no significant differences between the 2 groups in the incidence of total death, myocardial infarction, revascularization, and major adverse cardiac events up to 8 years.LVH in hypertensive patients who underwent successful PCI with DES was associated with higher incidence of cardiac death up to 8 years of follow-up. More careful managements and clinical follow-up are needed and treatment strategies should specifically focus to target prevention and reversal of LVH in hypertensive patients.

Impact of left ventricular hypertrophy on myocardial injury in patients with ST-segment elevation myocardial infarction.

Left ventricular hypertrophy (LVH) has been suggested as a determinant of outcome in patients with ST-segment elevation myocardial infarction (STEMI). However, available data are inconclusive and the underlying mechanisms remain unclear. Therefore, the aim of this study was to evaluate the impact of LVH on myocardial injury and clinical outcome in a large multicenter STEMI population. Cardiovascular magnetic resonance was performed in 795 patients within 10days after STEMI to assess left ventricular (LV) mass and parameters of myocardial injury. Gender-specific cutoff values of indexed LV mass were used to define LVH (67g/m2 for men and 61g/m2 for women). Rates of major adverse cardiac events (MACE) were determined at 12-month follow-up. LVH was present in 438 patients (55%) and associated with a significantly larger infarct size [18.3% of LV mass (%LV) versus 14.0%LV; p < 0.01], a lower myocardial salvage index (47.8 versus 54.4; p < 0.01), larger extent of microvascular obstruction (0.4 versus 0%LV; p < 0.01) and lower LV ejection fraction (47.9 versus 53.2%; p < 0.01) compared to STEMI patients without LVH. The effect of LVH on LV ejection fraction, infarct size and myocardial salvage index remained statistically significant after adjustment for baseline characteristics (p < 0.01 for all). MACE rates at 12 months were numerically higher in patients with versus without LVH without reaching statistical significance (7.5 versus 5.6%; p = 0.32). In STEMI patients, LVH is associated with more pronounced structural and functional alterations in CMR imaging as an indicator for adverse clinical outcomes in STEMI survivors.

THE IMPACT OF BASELINE LEFT VENTRICULAR HYPERTROPHY ON CLINICAL OUTCOMES IN THE PRECISION TRIAL

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular (CV) mortality. The PRECISION trial evaluated the CV safety of celecoxib and nonselective NSAIDs. We assessed the contemporary impact of LVH on CV outcomes diagnosed by EKG in this randomized clinical trial. We

TCT-489 Impact of Left Ventricular Hypertrophy on Coronary Artery Spasm as assessed by Acetylcholine Provocation Test

In our previous study, hypertensive patients with uncontrolled blood pressure had a significantly lower incidence of coronary artery spasm (CAS) than those with controlled blood pressure. However, it is unknown whether hypertensive patients with target-organ damage have a lower incidence of CAS than

Abstract 237: Prognostic Significance of Left Ventricular Hypertrophy (lvh) by Electrocardiography in a Minority-predominant Heart Failure (hf) Cohort

Background: Left ventricular Hypertrophy (LVH) has been associated with higher cardiovascular morbidity and mortality but most of these studies were conducted in majority (white) populations. LVH is known to be more common in African Americans (AA) who also have a higher prevalence of cardiovascular morbidity and mortality. The prognostic significance of LVH in AA with Heart Failure (HF) has not been well studied. Methods: We performed a retrospective analysis of a predominantly minority HF cohort (69.3% AA); after obtaining approval from our institutional review board. Our primary goal was to compare the HF outcomes [All-cause hospitalizations (ACH), hospitalizations primarily due to HF and ER visits] in patients with EKG evidence of LVH versus those without LVH. We also examined the racial (Blacks vs Whites), gender (males vs females) and age-based (≥60 Vs &lt;60 years) differential impact of LVH on HF outcomes and determined the prevalence of LVH in the cohort. Levene’s Test and t-test were used to analyze the data for equality of variances and means respectively. Result: Our HF cohort consisted of 599 patients (415 AA, 142 Caucasian, 22 others, 20 unknown). The prevalence of LVH in overall cohort was 26.7%. We noted that black had higher prevalence of LVH ( 31%) vs Whites (15.5%) while prevalence of LVH was not very different in males ( 27.9%) vs females( 25.7%) and ≥60 years of age( 27.5%) vs &lt;60 (27.3%). The analysis showed that there were statistically significant differences in the number of ACH (p-value = 0.014), HF hospitalizations (p-value = 0.019) and ER visits (p-value = 0.001) in the LVH group compared with the non-LVH group. . There were no racial, gender or age-based statistically significant differences in the impact of LVH on HF outcomes. Conclusion: Electrocardiographically determined LVH in a minority - predominant HF cohort is associated with worse outcomes. This needs to be prospectively validated in a larger cohort of HF and could serve as a prognostic marker to guide the care of HF patients.

CRT-400.08 Impact of Left Ventricular Hypertrophy in Hypertensive Patients Underwent Successful Percutaneous Coronary Intervention With Drug Eluting Stents on Long-term Clinical Outcomes

Hypertension (HTN) and its organ damage such as left ventricular hypertrophy (LVH) can lead to worsening heart failure, cardiovascular morbidity and mortality. However, there are limited data regarding the impact of LVH in HTN patients (pts) who underwent successful percutaneous coronary

Left ventricular hypertrophy on long-term cardiovascular outcomes in patients with ST-elevation myocardial infarction

Background: Left ventricular hypertrophy (LVH) had been associated with increased adverse cardiovascular events in hypertensive patients. Prognostic significance of LVH in patients with ST-elevation myocardial infarction (STEMI) is not established. This study aimed to investigate prognostic impact of LVH on the patients with STEMI. Methods: We analyzed the data and clinical outcomes of 30-day survivors with STEMI who underwent successful coronary intervention from 2003 to 2009. Definition of LVH was LV mass index (LVMI) >115 g/m2 in male and >95 g/m2 in female. Patients were classified into a LVH group and a non-LVH group. Occurrence of major adverse cardiovascular events (MACE; death, recurrent MI, target vessel revascularization (TVR)) within 5 years was evaluated. Results: We enrolled 418 patients and mean follow-up duration was 43 ± 17 months. Two hundred and fourteen patients (51%) had LVH. The survival of the patients with LVH was significantly worse than the patients without LVH (log-rank p = 0.024). In a multivariate regression model, the presence of LVH was independently associated with increased risk for all-cause mortality (OR, 2.37; 95% CI, 1.096–5.123, p = 0.028). When the end points were analyzed based on LVH severity, all-cause mortality was significantly correlated with LVH severity (p = 0.011). The severe LVH was independently associated with increased risk for all-cause mortality (OR, 5.110; 95% CI, 1.454–17.9, p = 0.001). Conclusion: LVH was associated with increased rate of adverse clinical outcomes in 30-day survivors after STEMI, who underwent successful coronary intervention.

Impact of Left Ventricular Hypertrophy on Survival in Chronic Obstructive Pulmonary Disease.

Left ventricular hypertrophy (LVH) is a significant cardiac risk factor, associated with increased mortality. The impact of LVH on mortality in chronic obstructive pulmonary disease (COPD) is unknown. We evaluated the impact of LVH on mortality in COPD patients by measurement of left ventricular dimensions by echocardiography. Retrospective cohort study utilizing a NHS database of COPD patients (TARDIS), in Tayside, Scotland (2001-2010), linked with databases regarding echocardiograms, pharmacy prescription, and the General Register Office for Scotland death registry. Cox proportional hazard regression was used to determine hazard ratios for mortality and hospital admissions based upon left ventricular mass index (LVMI) and left ventricular internal diastolic diameter after correction for all available influential covariates. Increased LVIDd was defined as >5.3 cm (female) and >5.9 cm (male). LVH was defined as an LVMI of >95 g/m(2) (female) and >115 g/m(2) (male). 617 patients were included for analysis. Mean (SD) age at diagnosis, 70 (9); mean FEV1 % (SD), 60.6 (19.3); mean resting SaO2 % (SD), 92.7 (10). Mean follow-up 4.5 years. Increased LVIDd was not associated with increased mortality, χ (2)= 0.767, p = 0.381. Increased LVMI was associated with a significant increased risk of mortality, χ (2) = 5.447, p = 0.02 with an adjusted HR (95 % CI) of 1.542 (1.068-2.228), p = 0.021. The presence of LVH, demonstrated by elevated left ventricular mass index is associated with a significantly increased risk of mortality in COPD patients. Therapeutic interventions are required to address this important modifiable risk factor in COPD patients.

Impact of left ventricular hypertrophy on troponin release during acute myocardial infarction: new insights from a comprehensive translational study.

BackgroundBiomarkers are frequently used to estimate infarct size (IS) as an endpoint in experimental and clinical studies. Here, we prospectively studied the impact of left ventricular (LV) hypertrophy (LVH) on biomarker release in clinical and experimental myocardial infarction (MI).Methods and ResultsST‐segment elevation myocardial infarction (STEMI) patients (n=140) were monitored for total creatine kinase (CK) and cardiac troponin I (cTnI) over 72 hours postinfarction and were examined by cardiac magnetic resonance (CMR) at 1 week and 6 months postinfarction. MI was generated in pigs with induced LVH (n=10) and in sham‐operated pigs (n=8), and serial total CK and cTnI measurements were performed and CMR scans conducted at 7 days postinfarction. Regression analysis was used to study the influence of LVH on total CK and cTnI release and IS estimated by CMR (gold standard). Receiver operating characteristic (ROC) curve analysis was performed to study the discriminatory capacity of the area under the curve (AUC) of cTnI and total CK in predicting LV dysfunction. Cardiomyocyte cTnI expression was quantified in myocardial sections from LVH and sham‐operated pigs. In both the clinical and experimental studies, LVH was associated with significantly higher peak and AUC of cTnI, but not with differences in total CK. ROC curves showed that the discriminatory capacity of AUC of cTnI to predict LV dysfunction was significantly worse for patients with LVH. LVH did not affect the capacity of total CK to estimate IS or LV dysfunction. Immunofluorescence analysis revealed significantly higher cTnI content in hypertrophic cardiomyocytes.ConclusionsPeak and AUC of cTnI both significantly overestimate IS in the presence of LVH, owing to the higher troponin content per cardiomyocyte. In the setting of LVH, cTnI release during STEMI poorly predicts postinfarction LV dysfunction. LV mass should be taken into consideration when IS or LV function are estimated by troponin release.

Impact of left ventricular hypertrophy on QT prolongation and associated mortality.

QT prolongation on electrocardiogram (ECG) is a risk marker of ventricular arrhythmias and all-cause mortality. Left ventricular hypertrophy (LVH) on ECG is also associated with poor outcome. Patients satisfying ECG voltage criteria for LVH frequently show concomitant QT prolongation. This study aimed to explore the impact of marked QT prolongation on all-cause mortality in patients copresenting with LVH voltage criteria and prolonged QT on ECG. We evaluated 3364 ECGs with corrected QT (QTc) interval ≥460 ms detected by Mayo Clinic's QT alert system from November 2010 through June 2011. Every ECG with QTc interval ≥460 ms was evaluated for the presence of LVH voltage criteria by using Sokolow-Lyon voltage, Cornell voltage, and Cornell product. Concomitant LVH voltage criteria were present in 181 of 3364 ECGs (5.3%) with QTc interval ≥460 ms. Mortality during a follow-up period of 217 ± 184 days was 13% (23 of 181). Independent of age and hypertension, the QTc interval predicted mortality in patients with LVH voltage criteria (hazard ratio 1.31 per 10-ms increase; 95% confidence interval 1.09-1.58; P < .01). Patients with LVH voltage criteria and QTc interval ≥500 ms had highest mortality (log rank, P < .001). The QTc interval was an independent predictor of mortality in patients with concomitant LVH voltage and prolonged QTc interval on ECG. Mortality was highest in those with QTc interval ≥500 ms. QT prolongation on ECGs with concomitant LVH voltage criteria should not be regarded as a harmless byproduct of LVH, but should be used as a significant marker of increased mortality risk similar to that in patients without LVH voltage criteria.

The impact of left ventricular hypertrophy on survival in candidates for liver transplantation

Left ventricular hypertrophy (LVH) occurs in 12% to 30% of patients with cirrhosis; however, its prognostic significance is not well studied. We assessed the association of LVH with survival in patients undergoing a liver transplantation (LT) evaluation. We performed a multicenter cohort study of patients undergoing an evaluation for LT. LVH was defined with transthoracic echocardiography. The outcome of interest was all-cause mortality. LVH was present in 138 of 485 patients (28%). Patients with LVH were older, more likely to be male and African American, and were more likely to have hypertension. Three hundred forty-five patients did not undergo transplantation (212 declined, and 133 were waiting): 36 of 110 patients with LVH (33%) died, whereas 57 of 235 patients without LVH (24%) died (P = 0.23). After LT, 8 of 28 patients with LVH (29%) died over the course of 3 years, whereas 9 of 112 patients without LVH (8%) died (P = 0.007). This finding was independent of conventional risk factors for LVH, and all deaths for patients with LVH occurred within 9 months of LT. No clinical or demographic characteristics were associated with mortality among LVH patients. In conclusion, the presence of LVH is associated with an early increase in mortality after LT, and this is independent of conventional risk factors for LVH. Further studies are needed to confirm these findings and identify factors associated with mortality after transplantation to improve outcomes.

The impact of left ventricular hypertrophy on survival in candidates for liver transplantation: LVH in Cirrhosis

The impact of left ventricular hypertrophy on survival in candidates for liver transplantation: LVH in Cirrhosis

Relationship of Multidirectional Myocardial Strain with Radial Thickening and Ejection Fraction and Impact of Left Ventricular Hypertrophy: A Study in a Community‐Based Cohort

Left ventricular (LV) systolic strain provides additional prognostic value to LV ejection fraction (LVEF) and wall motion analysis. However, the relationship between myocardial multidirectional strain and LVEF, and the effect of LV hypertrophy on this relationship, are not completely understood especially in unselected populations. LV global longitudinal (εL ) and circumferential (εC ) systolic strain analysis was performed by two-dimensional speckle tracking echocardiography in 215 participants from a community-based study. LV radial wall thickening was measured as global radial strain (εR ), and LVEF was assessed by biplane Simpson's method. εR was significantly associated with εC (β = -0.56, P < 0.01) and with εL (β = -0.18, P < 0.01). The contribution of εL to εR was especially evident in subjects with lower εC and in presence of LV hypertrophy (β = -0.30, P < 0.01). εL and εC were significantly associated with LVEF (β = -0.36 and β = -0.49, both P < 0.01) independent of LV mass and other confounders, and their interaction significantly improved the prediction of LVEF (R(2) -change = 0.14) but not of εR (R(2) -change = 0.002). εR is mainly related to εC with a smaller contribution of εL , which becomes especially evident in subjects with lower εC and in presence of LV hypertrophy. Therefore, radial thickening may not detect subclinical LV longitudinal function reduction in normal ventricles and when εC is preserved. While a reduction in εL has a limited impact on εR , it exerts a greater effect on global LVEF, therefore for a more accurate LVEF prediction both εL and εC need to be considered.