Changes in Left Ventricular Wall Movement after Acute Myocardial Infarction Measured by Reflected Ultrasound

Serial measurements of left ventricular posterior wall movement were made in eight patients with acute myocardial infarction by an ultrasound technique. Maximum posterior wall velocity and excursion were decreased during the first 36-hour period after infarction. In two patients a reduction in posterior wall velocity was associated with an increased pulmonary artery pressure and as the pressure returned towards normal the posterior wall motion also improved. It is suggested that this method provides a convenient, non-invasive bedside assessment of left ventricular function after acute myocardial infarction.     

Serum MMP-8: A Novel Indicator of Left Ventricular Remodeling and Cardiac Outcome in Patients after Acute Myocardial Infarction

Objective

Left ventricular (LV) remodeling following myocardial infarction (MI) is characterized by progressive alterations of structure and function, named LV remodeling. Although several risk factors such as infarct size have been identified, LV remodeling remains difficult to predict in clinical practice. Changes within the extracellular matrix, involving matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), are an integral part of left ventricular (LV) remodeling after myocardial infarction (MI). We investigated the temporal profile of circulating MMPs and TIMPs and their relations with LV remodeling at 1 year and clinical outcome at 3 years in post-MI patients.

Methods

This prospective multicentre study included 246 patients with a first anterior MI. Serial echocardiographic studies were performed at hospital discharge, 3 months, and 1 year after MI, and analysed at a core laboratory. LV remodeling was defined as the percent change in LV end-diastolic volume (EDV) from baseline to 1 year. Serum samples were obtained at hospital discharge, 1, 3, and 12 months. Multiplex technology was used for analysis of MMP-1, -2, -3, -8, -9, -13, and TIMP-1, -2, -3, -4 serum levels.

Results

Baseline levels of MMP-8 and MMP-9 were positively associated with changes in LVEDV (P = 0.01 and 0.02, respectively). When adjusted for major baseline characteristics, MMP-8 levels remained an independent predictor LV remodeling (P = 0.025). By univariate analysis, there were positive relations between cardiovascular death or hospitalization for heart failure during the 3-year follow-up and the baseline levels of MMP-2 (P = 0.03), MMP-8 (P = 0.002), and MMP-9 (P = 0.03). By multivariate analysis, MMP-8 was the only MMP remaining significantly associated with clinical outcome (P = 0.02).

Conclusion

Baseline serum MMP-8 is a significant predictor of LV remodeling and cardiovascular outcome after MI and may help to improve risk stratification.     

Late Ventricular Dysrhythmias after Myocardial Infarction

Serious ventricular dysrhythmias occurred in hospital after discharge from a coronary intensive care unit in 11 out of 142 patients with myocardial infarction. Previous rhythm changes, hypotension, and left ventricular failure were common findings; only one of these patients had an uneventful previous course. Four patients were resuscitated and left hospital; six were resuscitated but died at varying periods up to eight days after the event; one patient could not be resuscitated. Recent coronary occlusion or further myocardial infarction was demonstrated in 7 of these 11 patients and presumably accounted for the dysrhythmia.     

Suppression of Ventricular Tachyarrhythmias by Transvenous Intracardiac Pacing after Acute Myocardial Infarction

Transvenous intracardiac pacing was carried out on nine patients with recurrent ventricular tachyarrhythmia after drug treatment had failed. In eight patients recurrent Ventricular ectopic activity was suppressed by pacing at a rate above the sinus rate. With this technique the need for D.C. shock and repeated antiarrhythmic drugs can be avoided.     

Lignocaine Therapy for Ventricular Ectopic Activity after Acute Myocardial Infarction: A Double-blind Trial

The effectiveness of intravenous lignocaine in suppressing ventricular ectopic activity after acute myocardial infarction was examined in a double-blind trial in 82 patients. Whereas suppression of unifocal ventricular ectopics was achieved by lignocaine in 90% of patients, other forms of potentially more dangerous ectopic activity (multifocal or R-on-T ectopics) seemed more resistant to therapy. Cessation of ectopic activity was also observed in about one-third of the patients in the control group. The incidence of ventricular tachycardia and fibrillation and the mortality during and after the trial period were similar in the lignocaine-treated and control groups, whether or not the initial ventricular ectopics had been suppressed.This study provides no evidence to support the routine use of intravenous lignocaine in the management of ventricular ectopic activity after acute myocardial infarction.     

急性心肌梗死PCI术后早期T波倒置与左室功能的关系

目的:探讨急性ST段抬高心肌梗死直接PCI术后早期T波倒置与左心室功能的关系.方法:对急性ST段抬高心肌梗死直接PCI术后78例患者,以24小时抬高的T波是否倒置分组,采用超声心动描记术检测左室射血分数、心肌活动指数,评价早期T波倒置与左室功能的关系.结果:早期T波倒置组左心功能优于T波未倒置组(P＜0.01),T波深倒置组左心功能优于浅倒置组(P＜0.05).结论:急性ST段抬高心机梗死早期T波倒置可早期评估左心功能、判断预后.     

Pericarditis after Acute Myocardial Infarction

Fifty-two (6·8%) of 779 patients admitted to a coronary monitoring unit with acute myocardial infarction developed a pericardial friction rub. A diagnosis of postmyocardial infarction syndrome was made in three of these.The course of the 52 patients with pericarditis was compared with that of a consecutive series of 100 patients without pericarditis. As a group those with pericarditis manifested a longer period of pyrexia, a greater rise in serum enzymes, and a higher incidence of major arrhythmias and of radiological pulmonary oedema. The Peel prognostic index, however, did not differ significantly in the two groups. The hospital mortality of the pericarditis group was not significantly different from that of the 727 non-pericarditis patients. No specially adverse features were found in a follow-up of the pericarditis group.Though the presence of a pericardial rub in the first few days after a myocardial infarction may be a sign of extensive myocardial damage and is associated with a relatively high incidence of ventricular fibrillation, it does not appear to influence the hospital mortality of patients treated in a monitoring unit.     

N-乙酰半胱氨酸改善大鼠心肌梗死后心室结构重塑的研究

目的：探讨N-乙酰半胱氨酸（N-acetylcysteine,NAC）对大鼠心肌梗死（myocardial infarction,MI）后心室结构重塑的影响及其潜在机制。方法：Sprague-Dawley（SD）大鼠96只,随机分为空白对照组（blank control,BC组）6只,余90只制作心肌梗死模型,成功存活24小时后随机分为NAC干预组（NAC）34只,生理盐水对照组（NS）32只,NAC组腹腔注射NAC[0.2 mg·kg-1.2d-1],NS组腹腔注射同等剂量的生理盐水。连续干预4周后,超声心动图检测大鼠收缩期左室后壁厚度（systolic left ventricular posterior wallthickness,LVPW;s）,舒张期左室后壁厚度（diastolic left ventricular posterior wall thickness,LVPW;d）,收缩期室间隔厚度（systolicinterventricular septal thickness,IVS;s）,舒张期室间隔厚度（diastolic interventricular septal thickness,IVS;d）,左室质量指数（LV Mass）及校正后的左室质量指数（LV Mass Corrected）等,还原型谷胱甘肽（glutathione,GSH）和氧化型谷胱甘肽（glutathione disulfide,GSSG）检测试剂盒检测心肌组织中GSH的含量,并计算大鼠的存活率。结果：与BC组相比,NS组左室后壁厚度明显变薄,室间隔厚度显著减小,GSH含量明显减少,存活率明显下降,左室质量指数及校正后的左室质量指数明显增大,差异均具有显著统计学意义（P〈0.05）;NAC组左室后壁厚度、室间隔厚度等未见明显减小,左室质量指数及校正后的左室质量指数未见明显增大GSH含量未见明显降低,差异均不具有统计学意义（P〈0.05）,但存活率明显下降,差异具有统计学意义（P〈0.05）;与NS组相比,NAC组左室后壁厚度增厚,室间隔厚度显著提高,左室质量指数及校正后的左室质量指数明显减小,GSH含量明显增高,差异均具有统计学意义（P〈0.05）,但存活率无明显统计学差异（P〉0.05）。结论：NAC能改善大鼠心肌梗死后心室结构的重塑,可能与抑制氧化应激,增加GSH的含量有关,但其对心肌梗死后大鼠的存活率无明显影响。     

经皮冠脉介入手术时机的选择对急性心肌梗死患者左室重构及心功能的影响

目的:探讨手术时机的选择对急性心肌梗死患者行经皮冠脉介入手术后左室重构及心功能的影响。方法:选择2014年10月-2015年10月在我院接受经皮冠脉介入手术治疗的97例急性心肌梗死患者为研究对象,根据手术时间不同将患者分为急诊手术组(49例)和择期手术组(48例)。观察并比较两组患者手术前后平均二尖瓣压力差(mMPG)、肺动脉平均压(mPAP)、左室舒张末径(LVDEd)、左室收缩末径(LVSEd)、左房内径(LAd)以及半年内心衰再住院率。结果:手术前,两组患者心功能及血流动力学各指标比较,差异均无统计学意义(P0.05);手术后,两组患者LVDEd,LVSEd及LAd均低于手术前,且急诊手术组患者LVDEd,LVSEd及LAd均低于择期手术组,差异具有统计学意义(P0.05);手术后,两组患者mMPG及mPAP均低于手术前,且急诊手术组患者mMPG及mPAP均低于择期手术组,差异具有统计学意义(P0.05);急诊手术组患者术后6个月心衰再住院率(2.04%)低于择期手术组(6.25%),差异具有统计学意义(P0.05)。结论:手术时机的选择对于行经皮冠脉介入手术的急性心肌梗死患者具有重要意义。与择期手术效果相比,急诊手术能够更好地改善患者的心功能及左室重构,减少心衰再住院率,值得在临床推广应用。     

Myocardial Connective Tissue Growth Factor (CCN2/CTGF) Attenuates Left Ventricular Remodeling after Myocardial Infarction

Aims

Myocardial CCN2/CTGF is induced in heart failure of various etiologies. However, its role in the pathophysiology of left ventricular (LV) remodeling after myocardial infarction (MI) remains unresolved. The current study explores the role of CTGF in infarct healing and LV remodeling in an animal model and in patients admitted for acute ST-elevation MI.

Methods and Results

Transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) and non-transgenic littermate controls (NLC) were subjected to permanent ligation of the left anterior descending coronary artery. Despite similar infarct size (area of infarction relative to area at risk) 24 hours after ligation of the coronary artery in Tg-CTGF and NLC mice, Tg-CTGF mice disclosed smaller area of scar tissue, smaller increase of cardiac hypertrophy, and less LV dilatation and deterioration of LV function 4 weeks after MI. Tg-CTGF mice also revealed substantially reduced mortality after MI. Remote/peri-infarct tissue of Tg-CTGF mice contained reduced numbers of leucocytes, macrophages, and cells undergoing apoptosis as compared with NLC mice. In a cohort of patients with acute ST-elevation MI (n = 42) admitted to hospital for percutaneous coronary intervention (PCI) serum-CTGF levels (s-CTGF) were monitored and related to infarct size and LV function assessed by cardiac MRI. Increase in s-CTGF levels after MI was associated with reduced infarct size and improved LV ejection fraction one year after MI, as well as attenuated levels of CRP and GDF-15.

Conclusion

Increased myocardial CTGF activities after MI are associated with attenuation of LV remodeling and improved LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis.     

Lignocaine Therapy after Acute Myocardial Infarction

Thirty-five patients with ventricular dysrhythmias and seven with other dysrhythmias after acute myocardial infarction were treated with intravenous lignocaine.Satisfactory initial suppression of ventricular ectopic beats was achieved in 27 (82%) of 33 patients after either a 50-mg. bolus or a 50-mg. bolus followed by a 100-mg. bolus of intravenous 2% lignocaine. Continuous suppression of ventricular ectopic beats was accomplished in 21 (78%) of these 27 patients by continuous intravenous lignocaine infusions of 1 to 2 mg. per minute. Recurrence of ventricular ectopic beats occurred in four patients despite lignocaine infusion rates of up to 6 mg. per minute. Six patients with ventricular ectopic beats developed ventricular fibrillation despite satisfactory initial suppression of their dysrhythmia by lignocaine. In three of them ventricular fibrillation supervened while they were receiving a lignocaine infusion and two subsequently died. Unheralded ventricular fibrillation occurred in three other patients between four and seven days after completing the full course of lignocaine therapy.Toxic effects of lignocaine were minimal in patients receiving 1 to 2 mg. per minute.     

Circulating NOS3 Modulates Left Ventricular Remodeling following Reperfused Myocardial Infarction

Purpose

Nitric oxide (NO) is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3). We have shown that NO protects against myocardial ischemia/reperfusion (I/R) injury and that depletion of circulating NOS3 increases within 24h of ischemia/reperfusion the size of myocardial infarction (MI) in chimeric mice devoid of circulating NOS3. In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI.

Methods

To analyze the role of circulating NOS3 we transplanted bone marrow of NOS3^−/− and wild type (WT) mice into WT mice, producing chimerae expressing NOS3 only in vascular endothelium (BC−/EC+) or in both, blood cells and vascular endothelium (BC+/EC+). Both groups underwent 60 min of coronary occlusion in a closed-chest model of reperfused MI. During the 3 weeks post MI, structural and functional LV remodeling was serially assessed (24h, 4d, 1w, 2w and 3w) by echocardiography. At 72 hours post MI, gene expression of several extracellular matrix (ECM) modifying molecules was determined by quantitative RT-PCR analysis. At 3 weeks post MI, hemodynamics were obtained by pressure catheter, scar size and collagen content were quantified post mortem by Gomori’s One-step trichrome staining.

Results

Three weeks post MI, LV end-systolic (53.2±5.9μl;***p≤0.001;n = 5) and end-diastolic volumes (82.7±5.6μl;*p<0.05;n = 5) were significantly increased in BC−/EC+, along with decreased LV developed pressure (67.5±1.8mmHg;n = 18;***p≤0.001) and increased scar size/left ventricle (19.5±1.5%;n = 13;**p≤0.01) compared to BC+/EC+ (ESV:35.6±2.2μl; EDV:69.1±2.6μl n = 8; LVDP:83.2±3.2mmHg;n = 24;scar size/LV13.8±0.7%;n = 16). Myocardial scar of BC−/EC+ was characterized by increased total collagen content (20.2±0.8%;n = 13;***p≤0.001) compared to BC+/EC+ (15.9±0.5;n = 16), and increased collagen type I and III subtypes.

Conclusion

Circulating NOS3 ameliorates maladaptive left ventricular remodeling following reperfused myocardial infarction.     

Integrative Pathway-Centric Modeling of Ventricular Dysfunction after Myocardial Infarction

Background

A significant proportion of myocardial infarction (MI) patients undergo complex, coordinated perturbations at the molecular level that may eventually drive the occurrence of ventricular dysfunction and heart failure. Despite advances in the elucidation of key processes implicated in this condition, traditional methods relying on gene expression data and the identification of individual biomarkers in isolation pose major limitations not only for improving prediction power, but also for model interpretability. Mechanisms underlying clinical responses after MI remain elusive and there is no biomarker with the capacity to accurately predict ventricular dysfunction after MI. This calls for the exploration of system-level modeling of ventricular dysfunction in post-MI patients. Within this discovery framework key perturbations and predictive patterns are characterized by the integrated biological activity levels observed in pathways, rather than in individual genes.

Methodology/Principal Findings

Here we report an integrative approach to identifying pathways related with ventricular dysfunction post MI with potential prognostic and therapeutic value. We found that a diversity of pathway-level perturbations can be profiled in samples of patients with ventricular dysfunction post MI, most of which represent major reductions of gene expression. Highly perturbed pathways included those implicated in antigen-dependent B-cell activation and the synthesis of leucine. By analyzing patient-specific samples encoded with information derived from highly-perturbed pathways, it is possible to visualize differential prognostic patterns and to perform computational classification of patients with areas under the receiver operating characteristic curve above 0.75. We also demonstrate how the integration of the outcomes generated by different pathway-based analysis models may improve ventricular dysfunction prediction performance.

Significance

This research offers an alternative, comprehensive view of key relationships and perturbations that may trigger the emergence or prevention of ventricular dysfunction post-MI.     

血清同型半胱氨酸水平对急性ST段抬高型心肌梗死PCI术后患者左心室重构、心肌灌注和预后的影响

摘要 目的：探讨血清同型半胱氨酸（Hcy）水平与急性ST段抬高型心肌梗死（STEMI）患者经皮冠状动脉介入（PCI）术后左心室重构、心肌灌注以及预后的关系。方法：选择2018年2月至2020年1月我院收治的70例STEMI患者,根据入院时血清Hcy水平分为高水平Hcy组（Hcy＞30 μmol/L,41例）和低水平Hcy组（15≤Hcy≤30 μmol/L,29例）。PCI术后1个月、6个月、12个月检测左室重量指数(LVMI)和左心室射血分数(LVEF),复查冠脉造影,评价TIMI心肌灌注分级（TMPG）。Pearson相关或Spearman秩相关性分析Hcy水平与LVMI、LVEF、TMPG分级相关性。所有患者PCI术后随访12个月,记录患者随访期间全因死亡和主要不良心脏事件（MACE）发生情况。Cox风险比例回归分析PCI术后STEMI患者预后的影响因素。结果：高水平Hcy组PCI术后6、12个月 LVEF低于低水平Hcy组（P＜0.05）,LVMI高于低水平Hcy组（P＜0.05）,高水平Hcy组PCI术后心肌灌注不良发生率高于低水平Hcy组（P＜0.05）。Hcy水平与PCI术后6、12个月 LVEF呈负相关（P＜0.05）,与LVMI呈正相关（P＜0.05）,与PCI术后TMPG分级呈负相关（P＜0.05）。高水平Hcy组随访期间全因死亡和MACE发生率均高于低水平Hcy组（P＜0.05）。Cox风险比例回归分析结果显示Hcy、术前Gensini评分是STEMI患者PCI术后预后不良的影响因素（P＜0.05）。结论：高水平Hcy与STEMI患者PCI术后左心室重构、心肌灌注有关,且Hcy是STEMI患者PCI术后发生全因死亡和MACE的影响因素。     

心肌带收缩率与急性心肌梗死患者左心室收缩功能关系

目的:急性前壁心肌梗死明显影响室间隔收缩率和左心室射血分数(left ventricular ejection fraction LVEF)。本文旨在探讨心肌带降段及升段收缩率与急性前壁心肌梗死患者LVEF的相关性。方法:收集2015年4月-2017年2月在心内科住院的急性前壁心肌梗死患者36例,正常对照组患者39例。所有患者取左心室长轴M型超声心动图,测量室间隔收缩率、升段收缩率及降段收缩率。心肌梗死左心室射血分数采用双平面Simpson's法计算。结果:与正常对照组相比,心肌梗死组患者舒张末期心肌带升段厚度没有统计学差异(P=0.69),收缩末期升段厚度(P=0.014)更薄、升段收缩率(P0.01)明显降低;心肌梗死组舒张末期降段厚度(P0.01)更薄、收缩末期降段厚度(P0.01)更薄、降段收缩率(P0.01)明显降低;心肌梗死组左心室射血分数与降段收缩率(r~2=0.13,P=0.026)、室间隔增厚率(r~2=0.19,P0.01)呈正相关,与升段收缩率没有相关性(P0.05)。正常对照组左心室射血分数与室间隔增厚率、降段增厚率及升段增厚率无相关性。经过相关分析,筛选出与心肌梗死LVEF的相关因素,进一步经逐步回归分析,得多元线性回归方程为LVEF=48.206+18.914*LVDD(cm)-25.414*LVSD(cm)。结论:急性前壁心肌梗死室间隔降段收缩率明显受损,与左心室射血分数降低有关。多元线性回归方程可估算前壁心肌梗死LVEF。     

RT-3DE 评估急性心梗PCI术后左室收缩功能及同步性的临床价值

目的:探讨实时三维超声心动图技术(realtime three dimensional echocardiography,RT-3DE)对评价急性心肌梗死(acute myocardial infarction,AMI)经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)术后左室收缩功能及同步性的临床应用价值。方法:选择30例左室急性前壁及前间壁心梗并进行急诊PCI术的患者和30例正常对照组,应用Philips IE33彩色多普勒超声成像仪对PCI术前及术后1个月的左心室功能指标进行二维常规超声检查及三维超声心动图检查,应用Q-lab6.0软件进行分析。结果:二维超声心动图显示AMI组术前左心室收缩末容量(ESV)及舒张末容量(EDV)较对照组比较明显增大(P0.01),左心室射血分数(EF)较对照组明显减小(P0.01);急性心肌梗死(AMI)组术后1个月左心室ESV及EDV较术前比较减小(P0.05),左心室EF较术前增大(P0.05);AMI组术后1个月左心室ESV及EDV较对照组比较增大(P0.05),左心室EF较对照组减小(P0.05);三维超声心动图的各参数比较,AMI组PCI术前梗死节段局部收缩末期容量(RESV)及局部舒张末期容量(REDV)较对照组增大(P0.05),左心室梗死节段局部射血分数(REF)较对照组减小(P0.05);AMI组患者梗死节段RESV及REDV术后1个月较术前比较减小(P0.05),梗死节段REF较术前比较有所增大(P0.05),AMI组术后1个月梗死节段RESV及REDV较对照组增大(P0.05),梗死节段REF较对照组减小(P0.05);左室16节段从QRS波起点到最小收缩容积时间的标准差和最大差值(Tmsvl6-SD、Tmsvl6-Dif)以及用R-R间期校正后的Tmsvl6-SD%(左室收缩不同步指数systolic dyssynchrony index,SDI)和Tmsvl6-Dif%较术前比较减小(p0.05)。结论:PCI手术前、后应用RT-3DE能够准确评价左心室17节段的局部收缩功能及运动同步性,对AMI患者心功能的研究具有重要意义。     

结扎兔冠状动脉前降支与左室支的急性心肌梗塞比较

本文比较了结扎兔冠状动脉前降支（ＬＡＤ组）和左室支（ＬＶＡ组）两种方法建立的急性心肌梗塞模型。结果发现１：ＥＣＧ标测,三天内不同时间ＬＶＡ组∑△ＳＴ升高毫伏数均高于ＬＡＤ组（Ｐ＜０．０１或Ｐ＜０．０５）;２：Ｎ－ＢＴ染色,ＬＶＡ组心肌梗塞占心室重的百分率为１７．３％±０．５６％,而ＬＡＤ组为８．２％±２．４２％,两者相差非常显著（Ｐ＜０．０１）,证实了ＬＶＡ组心梗面积较ＬＡＤ组大且相对稳定。采用增强（Ｇｄ－ＤＴＰＡ）磁共振成像（ＭＲＩ）扫描发现ＬＶＡ组急性心梗范围在三天内基本稳定。作者认为,兔急性心梗模型采用结扎ＬＶＡ优于结扎ＬＡＤ。     

Association of Left Ventricular Mass with All-Cause Mortality,Myocardial Infarction and Stroke

Background

Our aim was to assess the association of left ventricular mass with mortality and nonfatal cardiovascular events.

Methodology/Principal Findings

Left ventricular mass was measured by echocardiography in 40138 adult patients (mean age 61.1±16.4 years, 52.5% male). The primary endpoint was all-cause mortality. Secondary endpoints included nonfatal myocardial infarction and nonfatal stroke. During a mean follow-up period of 5.6±3.9 years, 9181 patients died, 901 patients had a nonfatal myocardial infarction, and 2139 patients had a nonfatal stroke. Cumulative 10-year mortality was 26.8%, 31.9%, 37.4% and 46.4% in patients with normal, mildly, moderately and severely increased left ventricular mass, respectively (p<0.001). Ten-year rates of nonfatal myocardial infarction and stroke ranged from 3.2% and 6.7% in patients with normal left ventricular mass to 5.3% and 12.7% in those with severe increase in left ventricular mass, respectively. After multivariate adjustment, left ventricular mass remained an independent predictor of all-cause mortality (hazard ratio [HR] per 100 g increase 1.21, 95% confidence interval [CI] 1.14–1–27, p<0.001 in women, and HR 1.09, 95% CI 1.04–1–13, p<0.001 in men), myocardial infarction (HR 1.60, 95% CI 1.31–1.94, p<0.001 in women and HR 1.15, 95% CI 1.02–1.29, p = 0.019 in men) and stroke (HR 1.26, 95% CI 1.13–1.40, p<0.001 in women and HR 1.19, 95% CI 1.09–1.30, p<0.001 in men).

Conclusions/Significance

Left ventricular mass has a graded and independent association with all-cause mortality, myocardial infarction and stroke.