The relationship between renal function and cardiac structure, function, and prognosis after myocardial infarction: the VALIANT Echo Study.

OBJECTIVES: The purpose of this study was to determine whether alterations in cardiac structure or function contribute to the increased risk associated with renal impairment after myocardial infarction (MI). BACKGROUND: Renal impairment is associated with adverse cardiovascular outcomes after MI. METHODS: Echocardiography was performed on 603 patients with left ventricular (LV) dysfunction, heart failure (HF), or both after MI. Patients were grouped according to their estimated glomerular filtration rate (eGFR), and measures of cardiac structure and function were related to baseline eGFR. The relationship between eGFR and cardiac structure and function and clinical outcomes of death or HF was assessed with multivariable Cox regression. RESULTS: Ejection fraction, infarct segment length, right ventricular function, and mitral deceleration time were not influenced by renal function. Patients with reduced eGFR had smaller LV and larger left atrial (LA) volumes and higher left ventricular mass index (LVMI) and LV mass/LV volume ratio. A greater proportion of the patients with reduced eGFR had LV hypertrophy. The relationship between eGFR and the outcome of death or HF was attenuated by including baseline differences in LVMI, and both LVMI and LA volume conferred additional prognostic information in a multivariable model. CONCLUSIONS: Renal impairment was associated with smaller LV and larger LA volumes and increased LVMI. Systolic function was similar when compared with patients with normal renal function. Thus, reduced systolic function cannot account for worse outcomes in patients with renal impairment after MI. Indirect measures of diastolic function suggest that diastolic dysfunction might be an important mediator of increased risk in this population.     

Left atrial remodelling in patients with myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALIANT Echo Study

Aims: To assess the relationship between left atrial (LA) size andoutcome after high-risk myocardial infarction (MI) and to studydynamic changes in LA size during long-term follow-up. Methods and results: The VALIANT Echocardiography study prospectively enrolled 610patients with left ventricular (LV) dysfunction, heart failure(HF), or both following MI. We assessed LA volume indexed tobody surface area (LAVi) at baseline, 1 month, and 20 monthsafter MI. Baseline LAVi was an independent predictor of all-causedeath or HF hospitalization (P = 0.004). In patients who survivedto 20 months, LAVi increased a mean of 3.00 ± 7.08 mL/m²from baseline. Hypertension, lower estimated glomerular filtrationrate, and LV mass were the only baseline independent predictorsof LA remodelling. Changes in LA size were related to worseningin MR and increasing in LV volumes. LA enlargement during thefirst month was significantly greater in patients who subsequentlydied or were hospitalized for HF than in patients without events. Conclusion: Baseline LA size is an independent predictor of death or HFhospitalization following high-risk MI. Moreover, LA remodellingduring the first month after infarction is associated with adverseoutcome.     

Adverse effects of right ventricular pacing on cardiac function: prevalence,prevention and treatment with physiologic pacing

Right ventricular (RV) pacing is the main treatment modality for patients with advanced atrioventricular (AV) block. Chronic RV pacing can cause cardiac systolic dysfunction and heart failure (HF). In this review, we discuss studies that have shown deleterious effects of chronic RV pacing on systolic cardiac function causing pacing-induced cardiomyopathy (PiCM), heart failure (HF), HF hospitalization, atrial fibrillation (AF) and cardiac mortality. RV apical pacing is the most widely used and studied. Adverse effects of RV pacing appear to be directly related to pacing burden and are worse in patients with pre-existing left ventricular (LV) dysfunction. Chronic RV pacing is also associated with heart failure with preserved ejection fraction (HFpEF). Mechanisms, risk factors, clinical and echocardiographic features, and strategies to minimize RV pacing-induced cardiac dysfunction are discussed in light of the latest data. Studies on biventricular (Bi-V) pacing upgrade in patients who develop RV PiCM, use of alternate RV pacing sites, de novo Bi-V pacing, and physiologic pacing using HIS bundle pacing (HBP) and left bundle area (LBBA) pacing in patients with an anticipated high RV pacing burden are discussed.     

抑制诱生型一氧化氮合酶对大鼠心肌梗死后左心室形态及心功能的影响

目的 :探讨抑制诱生型一氧化氮合酶 (iNOS)对大鼠心肌梗死后左心室形态及心功能的影响。方法 :结扎大鼠左冠状动脉建立心肌梗死模型。免疫组化检测心肌iNOS表达水平。分别于心肌梗死发生前、心肌梗死 7d后开始iNOS抑制剂S methylisothiourea (SMT)干预 ,于心肌梗死 6周后测定血浆一氧化氮 (NO)、心肌iNOS表达、左心室形态变化和心功能。结果 :心肌梗死 6周后心肌iNOS表达增加 ,血浆NO水平上升。于心肌梗死发生前、心肌梗死 7d后开始SMT干预均可降低血浆NO水平 ,减轻心室扩张 ,减轻心室重量 ,改善心功能。心肌梗死发生前开始SMT干预尚可提高存活率。结论 :iNOS在心肌梗死后心功能障碍的发生发展过程中起促进作用 ,抑制iNOS可以改善左心室功能 ,其机制与减轻心肌梗死后左心室重构有关。     

Cardiac imaging to identify patients at risk for developing heart failure after myocardial infarction

The development of heart failure (HF) after acute myocardial infarction (MI) is recognized as a major complication that leads to a significant increase in morbidity and mortality. Given the availability of effective treatments for improving both quality of life and survival for patients at increased risk for developing HF after MI, early identification of these individuals is critical. Noninvasive cardiac imaging offers a detailed characterization of two important pathophysiological processes related to the development of HF post-MI: left ventricular (LV) remodeling and LV functional recovery. Cardiovascular MRI has recently emerged as the preferred noninvasive imaging modality because of its ability to provide the most comprehensive and informative evaluation of these processes. In addition to allowing for an accurate and reproducible longitudinal follow-up of LV volumes and mass, MRI also offers information on infarct size, the presence of microvascular obstruction, and the transmural extent of infarct scar, all of which are valuable parameters that can assist in identifying patients at risk for developing HF after MI.     

Vasodilatory action of endogenous atrial natriuretic factor in a rat model of chronic heart failure as determined by monoclonal ANF antibody

Elucidation of the role of (elevated) endogenous atrial natriuretic factor (ANF) in chronic heart failure has been hampered by a lack of specific inhibitors. We used a newly developed monoclonal antibody that has been shown to specifically block both exogenously and endogenously released ANF in vivo. For assessment of the vasodilatory action of ANF in chronic heart failure, either this antibody against ANF or ascites (control serum) was injected in rats with myocardial infarction and failure and in sham animals. Ascites did not alter central hemodynamics in either the sham or infarcted group. Antibody significantly increased right atrial pressure, left ventricular end-diastolic pressure, and systemic vascular resistance (SVR) in the infarction group but did not affect these variables in the sham group. Because renal blood flow, as measured by radioactive microspheres, decreased significantly in all four groups, probably due to nonspecific renal vasoconstrictor effects of the ascites, a separate group of infarcted animals was treated with purified ANF antibody (devoid of nonspecific effects) or mouse IgG as a control injection. In these animals, right atrial pressure increased from 1.1 +/- 0.7 to 2.6 +/- 0.7 mm Hg (p less than 0.001). Although SVR, renal blood flow velocity (measured by Doppler probe), and renal vascular resistance did not change in the infarcted animals after administration of purified ANF antibody, a significant correlation was found between baseline plasma ANF values and the change in SVR exerted by purified ANF antibody (r = 0.758, p less than 0.02, n = 9); that is, SVR increased in rats with high baseline plasma ANF (greater than 350 pg/ml), but decreased in animals with plasma ANF less than 200 pg/ml. These results suggest that moderately elevated endogenous plasma ANF levels in chronic heart failure do affect central hemodynamics, primarily by reducing venous pressure (e.g., by decreasing intravascular volume or by venous dilation). Arterial vasodilation, however, appears to emerge when plasma ANF is greatly increased.     

Prevention of adverse electrical and mechanical remodeling with biventricular pacing in a rabbit model of myocardial infarction.

BACKGROUND: Biventricular (BIV) pacing can improve cardiac function in heart failure (HF). OBJECTIVE: This study sought to investigate the mechanisms of benefit of BIV pacing using a rabbit model of myocardial infarction (MI). METHODS: New Zealand White rabbits were divided into 4 groups (sham-operated [C], MI with no pacing [MI], MI with right ventricular pacing [MI+RV], and MI with BIV pacing [MI+BIV]) and underwent serial electrocardiograms and echocardiograms. At 4 weeks, hearts were excised and tissue was extracted from various areas of the left ventricle (LV). RESULTS: Four weeks after coronary ligation, BIV pacing prevented systolic and diastolic dilation of the LV as well as the reduction in its fractional shortening, restored the QRS width and the rate-dependent QT intervals to their baseline values, and prevented the decline of the ether-a-go-go (Erg) protein levels. This prevention of remodeling was not documented in the MI+RV groups. CONCLUSION: In this rabbit model of BIV pacing and MI, we show prevention of adverse mechanical and electrical remodeling of the heart. These changes may underlie some of the benefits seen with BIV pacing in HF patients with more severe LV dysfunction.     

Angiotensin II receptor blockade attenuates the deleterious effects of exercise training on post-MI ventricular remodelling in rats

OBJECTIVES: The effects of exercise training on LV remodelling following large anterior myocardial infarction (MI) remains controversial. Blockade of the renin-angiotensin system has been shown to prevent ventricular dilation and deleterious remodeling. We therefore tested, in a rat model of chronic MI, whether any potentially deleterious effects of exercise on post-MI remodelling could be ameliorated by angiotensin II receptor blockade. METHODS: Male Wistar rats underwent coronary ligation or sham operation. Treatment with losartan (10 mg/kg/day) began 1 week post-MI and moderate treadmill exercise (25 m/min, 60 min/day, 5 days/week) was initiated 2 weeks post-MI. Systolic and diastolic pressure-volume relationships were measured in isolated, red-cell perfused, isovolumically beating hearts 8 weeks post-MI. Morphometric measurements were performed in trichrome stained cross sections of the heart. Five groups of animals were compared: sham (n=13), control MI (MI; n=11), MI plus losartan (MI-Los; n=13), MI plus exercise (MI-Ex; n=10) and MI plus exercise and losartan (MI-Ex-Los; n=12). RESULTS: Infarct size (% of left ventricle, LV) was similar among the infarcted groups [MI=43+/-4%, MI-Los=49+/-2%, MI-Ex=45+/-1%, MI-Ex-Los=48+/-2% (NS)]. Exercise, losartan and exercise+losartan treatments all attenuated LV dilation post-MI to a similar degree. Exercise training increased LV developed pressure in both untreated and losartan treated hearts (P<0.05 vs. other MI groups). In addition, exercise resulted in additional scar thinning in untreated hearts, while no additional scar thinning was seen in post-infarct hearts receiving both losartan and exercise. CONCLUSIONS: Following large anterior MI, losartan attenuated LV dilation and scar thinning. In untreated animals, exercise decreased dilation, but also contributed to scar thinning. Therefore, exercise concurrent with blockade of the renin-angiotensin system may provide optimal therapeutic benefit following large anterior MI.     

Exercise promotes angiogenesis and improves beta-adrenergic receptor signalling in the post-ischaemic failing rat heart

AIMS: We investigated whether exercise training could promote angiogenesis and improve blood perfusion and left ventricular (LV) remodelling of the post-myocardial infarction (MI) failing heart. We also explored the contribution of ameliorated beta-adrenergic receptor signalling and function on the overall improvement of cardiac contractility reserve induced by exercise. METHODS AND RESULTS: Adult Wistar male rats were randomly assigned to one of four experimental groups. Sham-operated and post-MI heart failure (HF) rats were housed under sedentary conditions or assigned to 10-weeks of a treadmill exercise protocol. At 4 weeks after MI, sedentary HF rats showed LV eccentric hypertrophy, marked increase of LV diameters associated with severely impaired fractional shortening (14 +/- 5%), increased LV end diastolic pressure (20.9 +/- 2.6 mmHg), and pulmonary congestion. In addition, cardiac contractile responses to adrenergic stimulation were significantly blunted. In trained HF rats, exercise was able to (i) reactivate the cardiac vascular endothelial growth factor pathway with a concurrent enhancement of myocardial angiogenesis, (ii) significantly increase myocardial perfusion and coronary reserve, (iii) reduce cardiac diameters, and (iv) improve LV contractility in response to adrenergic stimulation. This latter finding was also associated with a significant improvement of cardiac beta-adrenergic receptor downregulation and desensitization. CONCLUSIONS: Our data indicate that exercise favourably affects angiogenesis and improves LV remodelling and contractility reserve in a rat model of severe chronic HF.     

Contribution of the ventricles and the atrial appendages to the elevation of plasma atrial natriuretic factor (ANF) during pacing-induced heart failure in conscious dogs

The goal of our study was to determine whether the elevation in plasma ANF was produced by the atrial appendages or ventricular tissue during pacing-induced heart failure in chronically instrumented conscious dogs (sham) or dogs with bilateral atrial appendectomy. Acute volume expansion caused a significant elevation of plasma ANF from 80±8 to 149±26 pg/ml (p<0.01) in sham dogs, but caused no significant change from 67±7 to 84±8 pg/ml in atrial appendectomized dogs. There were increases in left ventricular end-diastolic pressure (LVEDP) and left atrial pressure (LAP) in both groups of dogs. After rapid left ventricular pacing (210–240 beats/min) for 4 weeks to induce heart failure, dogs in both groups had tachycardia, elevated LVEDP and higher LAP. Plasma ANF was increased by 250% to 283±64 pg/ml (p<0.01) in sham dogs, and only 40% to 94±15 pg/ml (p>0.05) in atrial appendectomized dogs. In response to volume expansion, there were further increases in LVEDP and LAP in both groups of dogs, but plasma ANF was not elevated (288±39 pg/ml) in sham dogs and only slightly increased (132±7 pg/ml) in atrial appendectomized dogs. Our results suggest that, during pacing-induced heart failure, the atrial appendages are the major source of elevated plasma ANF, and the remaining atrial and ventricular tissue, even when maximally stretched, can only modestly increase plasma ANF.Supported by PO-1-HL 43023 from the Heart, Lung and Blood Institute     

Left ventricular SERCA2a gene down-regulation does not parallel ANP gene up-regulation during post-MI remodelling in rats

BACKGROUND: In most animal models of chronic hemodynamic overload of the left ventricle (LV) as well as in human end stage heart failure, the sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a) mRNA levels are decreased in parallel with increased atrial natriuretic peptide (ANP) mRNA levels. The situation in the remote myocardium following myocardial infarction (MI) is unclear. AIMS: (1) To examine SERCA2a mRNA levels in the non-infarcted LV myocardium of rats at the chronic stage of experimental MI and (2) To examine whether a negative linear correlation exists between SERCA2a and ANP mRNA levels in this model. METHODS: Anesthetized adult male Wistar rats underwent left coronary artery ligation or sham operation. Three months later, the rats were divided into three groups: sham-operated rats (sham, n=21), HF-free rats with MI (non-failing (NF)-MI, n=29) and rats with both MI and HF (congestive heart failure (CHF)-MI, n=14). LV remodelling and function were assessed by echocardiography and hemodynamic measurements. SERCA2a and ANP mRNA levels were determined by Northern and dot blot analysis with specific cDNA probes. RESULTS: LV SERCA2a mRNA levels varied markedly in sham-operated rats (0.9-1.8). Mean ANP mRNA level increased markedly and mean SERCA2a mRNA level decreased moderately in the remote myocardium. In some NF-MI rats, SERCA2a mRNA levels were higher than those in some sham controls. Whereas ANP mRNA levels correlated well with MI severity (r2=0.79, p<0.001), this was not the case for SERCA2a mRNA levels (r2=0.42, p<0.01). We found no negative correlation between ANP and SERCA2a mRNA levels. CONCLUSION: SERCA2a gene down-regulation in the non-infarcted myocardium of rats with MI does not correlate with ANP gene up-regulation, suggesting that the two genes are not antithetically regulated.     

Genetic basis for chamber-specific ventricular phenotypes in the rat infarct model

BACKGROUND: We, and others, have previously reported a strong correlation between increased inter-ventricular dispersion of repolarization and the occurrence of fatal arrhythmia in animal models of CHF. The existence of this and other such distinct electrophysiologic phenotypes in right (RV) vs. left ventricles (LV) could be explained by chamber-specific patterns of gene expression. METHODS: We employed microarray gene profiling of 13824 sequence-verified, nonredundant rodent cDNAs to compare myocardial gene expression in RV vs. LV of rats with surgically induced myocardial infarction (MI: n=3) and in sham-operated animals (Sham: n=3). RESULTS: Significant LV infarction (32+/-4% LV) and severe CHF were observed in all MI animals at 4 weeks. In Sham animals, 937 genes exhibited significant differential expression in RV vs. LV myocardium. In MI animals, 1158 genes exhibited significant differential expression in RV vs. LV. Of those genes exhibiting significant differential expression, only 241 were common to both Sham and MI animals. Differentially expressed genes included those involved in signal transduction, cell growth and maintenance, and apoptosis. Genes with potential roles in altered dispersion of repolarization included voltage-dependent Ca(2+) channel gamma subunit (MI 8-fold increasing) and K(+) inwardly rectifying channel subfamily J, member 10 (MI 6-fold decreasing). Gap junction membrane channel protein alpha 4 (MI 6-fold decreasing) and cardiac troponin I (MI 8-fold decreasing) were also significantly differentially expressed. Inter-ventricular comparisons revealed significantly greater alterations in gene expression vs. intra-ventricular comparisons. CONCLUSIONS: Microarray gene profiling has revealed candidate genes, some of them novel, which may account for chamber-specific ventricular electrophysiologic phenotypes, both in physiologic as well as in arrhythmogenic states such as CHF.     

Right and left ventricular activation sequence in patients with heart failure and right bundle branch block: a detailed analysis using three-dimensional non-fluoroscopic electroanatomic mapping system

Three-dimensional mapping in RBBB and heart failure. INTRODUCTION: Recently, right bundle branch block (RBBB) was proved to be an important predictor of mortality in heart failure (HF) patients as much as left bundle branch block (LBBB). We characterized endocardial right ventricular (RV) and left ventricular (LV) activation sequence in HF patients with RBBB using a three-dimensional non-fluoroscopic electroanatomic contact mapping system (3D-Map) in order to provide the electrophysiological background to understand whether these patients can benefit from cardiac resynchronization therapy (CRT). METHODS AND RESULTS: Using 3D-Map, RV and LV activation sequences were studied in 100 consecutive HF patients. Six of these patients presented with RBBB QRS morphology. The maps of these patients were analyzed and compared post hoc with those of the other 94 HF patients presenting with LBBB. Clinical and hemodynamic profile was significantly worse in RBBB group compared to LBBB. Patients with RBBB showed significantly longer time to RV breakthrough (P<0.001), longer activation times of RV anterior and lateral regions (P<0.001), and longer total RV endocardial activation time (P<0.02) compared to patients with LBBB. Time to LV breakthrough was significantly shorter in patients with RBBB (P<0.001), while total and regional LV endocardial activation times were not significantly different between the two groups. CONCLUSIONS: Degree of LV activation delay is similar between HF patients with LBBB and RBBB. Moreover, patients with RBBB have larger right-sided conduction delay compared to patients with LBBB. The assessment of these electrical abnormalities is important to understand the rationale for delivering CRT in HF patients with RBBB.     

Right ventricular dysfunction and risk of heart failure and mortality after myocardial infarction

OBJECTIVES: The aim of this study was to determine the prognostic value of right ventricular (RV) function in patients after a myocardial infarction (MI). BACKGROUND: Right ventricular function has been shown to predict exercise capacity, autonomic imbalance and survival in patients with advanced heart failure (HF). METHODS: Two-dimensional echocardiograms were obtained in 416 patients with left ventricular (LV) dysfunction (ejection fraction [LVEF] < or = 40%) from the Survival And Ventricular Enlargement (SAVE) echocardiographic substudy (mean 11.1 +/- 3.2 days post infarction). Right ventricular function from the apical four-chamber view, assessed as the percent change in the cavity area from end diastole to end systole (fractional area change [FAC]), was related to clinical outcome. RESULTS: Right ventricular function correlated only weakly with the LVEF (r = 0.12, p = 0.013). On univariate analyses, the RV FAC was a predictor of mortality, cardiovascular mortality and HF (p < 0.0001 for all) but not recurrent MI. After adjusting for age, gender, diabetes mellitus, hypertension, previous MI, LVEF, infarct size, cigarette smoking and treatment assignment, RV function remained an independent predictor of total mortality, cardiovascular mortality and HF. Each 5% decrease in the RV FAC was associated with a 16% increased odds of cardiovascular mortality (95% confidence interval 4.3% to 29.2%; p = 0.006). CONCLUSIONS: Right ventricular function is an independent predictor of death and the development of HF in patients with LV dysfunction after MI.     

心肌梗死致心肌瘢痕患者与二尖瓣关闭不全程度的关系

目的:缺血性二尖瓣关闭不全是由缺血性心肌病引起的左心室重构,瓣叶牵拉所导致。本研究通过心脏核磁延迟强化成像分析左心室心肌瘢痕对冠心病患者发生中重度缺血性二尖瓣关闭不全的预测作用。方法:本研究回顾性分析2015年1月1至2018年12月31日,在北京安贞医院就诊的冠心病患者,共有111例患者符合入排标准入选本研究。应用心脏核磁延迟强化成像定量技术,计算左心室心肌瘢痕总量,乳头肌瘢痕及左心室前壁、间隔壁、下壁、侧壁瘢痕量。应用Logistic回归分析探索与冠心病患者发生中重度缺血性二尖瓣关闭不全相关的左心室心肌瘢痕情况。结果:多因素Logistic回归结果分析提示:左心室心肌瘢痕总量(RR=1.02,95%CI:1.002~1.03,P<0.05)及乳头肌瘢痕(RR=3.45,95%CI:1.03~11.58,P<0.05)与冠心病患者发生中重度缺血性二尖瓣关闭不全相关,而左心室各壁瘢痕量与冠心病发生中重度缺血性二尖瓣关闭不全无相关性。结论:左心室心肌瘢痕总量及乳头肌瘢痕是冠心病患者发生中重度缺血性二尖瓣关闭不全的危险因素。     

Myocardial bradykinin B2-receptor expression at different time points after induction of myocardial infarction

OBJECTIVE: To characterize the regulation of the myocardial bradykinin B2 receptor after induction of myocardial infarction (MI), we studied its expression at different time points in the left ventricle (LV), right ventricle (RV) and interventricular septum (S) of the heart. DESIGN: Male Sprague-Dawley rats were submitted to permanent occlusion of the left descending coronary artery. Six hours, 24 h or 6 days after MI induction or a sham operation, a Millar-tip catheter was placed in the LV. Left ventricular pressure (LVP) and contractility [(dP/dt)max] were measured. The LV, RV and S of all animals were isolated, and total RNA was extracted. B2-receptor expression was analysed by an RNase-protection assay. In addition, Western blot analysis was used to determine protein levels of the B2 receptor in the infarcted area of the LV. RESULTS: We observed a decrease in LVP and contractility at all time points after MI in comparison with sham-operated animals. Basal B2-receptor expression was detected in the LV and RV, but not in the S of sham-operated rats. In the LV of infarcted hearts, we found a time-dependent up-regulation of the B2-receptor expression, which was increased twofold and fivefold, respectively, 6 h and 24 h after induction of MI compared with controls. This increase was maintained for at least 6 days. Similarly, we also found an up-regulation of the B2-receptor expression in the RV and S. Both reached a peak 24 h after induction of MI. The protein level of the receptor gradually increased up to day 6. CONCLUSION: We conclude that myocardial ischaemia triggers B2-receptor up-regulation in both the infarcted and non-infarcted areas of the heart.     

Associations of right ventricular pulsatile load and cardiac power output to clinical outcomes in heart failure: Difference from systemic circulation

BackgroundAlthough left ventricular (LV) cardiac power output (CPO) is a powerful prognostic indicator in heart failure (HF), the significance of right ventricular (RV) CPO is unknown. In contrast, RV pulsatile load is a key prognostic marker in HF. We investigated the impact of RV-CPO and pulsatile load on cardiac outcome and the prognostic performance of the combined systemic and pulmonary circulation parameters in HF.MethodsRight heart catheterization and echocardiography were performed in 231 HF patients (62 ± 16 years, LV ejection fraction 42 ± 18 %). Invasive and noninvasive CPOs were calculated from mean systemic or pulmonary arterial pressure and cardiac output. LV-CPO was then normalized to LV mass (LV-P/M). Pulmonary arterial capacitance and the ratio of acceleration time to ejection time (AcT/ET) of RV outflow were used as parameters of RV pulsatile load. The primary endpoints, defined as a composite of cardiac death, HF hospitalization, ventricular arrythmia, and LVAD implantation after the examination, were recorded.ResultsNoninvasive CPOs were moderately correlated with invasive ones (LV: ρ = 0.787, RV: ρ = 0.568, and p < 0.001 for both). During a median follow-up period of 441 days, 57 cardiovascular events occurred. Lower LV-P/M and higher RV pulsatile load were associated with cardiovascular events; however, RV-CPO was not associated with the outcome. Echocardiographic LV-P/M and AcT/ET showed significant incremental prognostic value over the clinical parameters.ConclusionsRV pulsatile load assessed by AcT/ET may be a predictor of clinical events in HF patients. The combination of echocardiographic LV-P/M and AcT/ET could be a novel noninvasive prognostic indicator in HF patients.     

Long-term survival using intra-aortic balloon pump and percutaneous right ventricular assist device for biventricular mechanical support of cardiogenic shock

Right ventricular (RV) involvement in acute inferior left ventricular (LV) myocardial infarction increases the risks of cardiogenic shock and in-hospital mortality. Acutely impaired RV performance results in reduced LV preload and, in combination with impaired LV contractility, causes severely reduced LV stroke volume and cardiac output. Here we report long-term patient survival after acute biventricular myocardial infarction (MI) using simultaneous RV support with a TandemHeart percutaneous ventricular assist device (Cardiac Assist Technologies, Pittsburgh, Pennsylvania) and LV support with an intra-aortic balloon pump. Further evaluation of completely percutaneous biventricular support in acute MI is warranted.     

Prevention of cardiac remodeling after myocardial infarction in transgenic rats deficient in brain angiotensinogen

The brain renin-angiotensin-aldosterone system (RAAS) plays a major role in cardiac remodeling after myocardial infarction (MI). To assess the contribution of the brain RAAS in the activation of the cardiac RAAS post-MI, transgenic (TG) rats deficient in brain angiotensinogen and Wistar rats with intracerebroventricular (ICV) infusion of spironolactone were studied. An MI was induced by acute coronary artery ligation. TG and control Sprague-Dawley (SD) rats were followed for 8 weeks and Wistar rats for 6 weeks. Infarct sizes, % of left ventricle (LV) area, were in the 30-33% range. In SD rats at 8 weeks post-MI, internal circumference, interstitial and perivascular fibrosis, cardiomyocyte diameter in the LV and right ventricle (RV), laminin and fibronectin in the LV, and lung weights were increased. Aldosterone was increased markedly in both the LV and RV at 8 weeks post-MI. In TG rats, the MI-induced increases of RV internal circumference and weight were prevented and increases of lung weight and LV internal circumference were significantly inhibited. In TG rats, the post-MI increases of interstitial fibrosis and cardiomyocyte diameter were prevented in septum and RV and significantly inhibited in the peri-infarct zone of the LV. The increases in perivascular fibrosis, laminin and fibronectin were prevented in the LV. In TG rats, cardiac aldosterone did not increase. In Wistar rats at 6 weeks post-MI, aldosterone was markedly increased in the LV, but not in the RV. This increase was prevented by ICV infusion of spironolactone. These findings support the pivotal role of locally produced angiotensin II in the brain in cardiac remodeling post-MI. The brain RAAS appears to activate a cascade of events, among others an increase in cardiac aldosterone, which play a major role in cardiac remodeling post-MI.