Postischemic Left Ventricular Dysfunction Is Abolished by Alpha-Adrenergic Blocking Agents

Objectives. We sought to evaluate the efficacy of alpha-adrenergic blocking agents in counteracting left ventricular (LV) dysfunction occurring after transient ischemia in humans.Background. The mechanisms underlying postischemic LV dysfunction are largely unknown.Methods. Percutaneous transluminal coronary angioplasty (PTCA) provides a clinical model of ischemia and reperfusion. In 50 patients undergoing coronary stenting for 77 ± 5% stenosis, LV function was monitored by transesophageal echocardiography during and 30-min after PTCA. Fifteen minutes after stenting, 15 patients received 12 μg/kg body weight of the alpha-blocker phentolamine intracoronarily, 15 patients received 600 μg/kg of the alpha₁-blocker urapidil intravenously, 10 patients received the combination of phentolamine and 1.2 mg of propranolol intracoronarily, and 10 patients received saline.Results. Fifteen minutes after successful coronary dilation, significant contractile dysfunction occurred in previously ischemic and nonischemic myocardium. LV dysfunction was accompanied by an increase in coronary resistance and diffuse vasoconstriction. Alpha-blockers counteracted LV dysfunction and coronary resistance and the increase in vasoconstriction. Phentolamine and urapidil increased global LV shortening from 34 ± 9% to 45 ± 8% and to 49 ± 8%, respectively (p < 0.05). After the administration of propranolol combined with phentolamine, LV dysfunction remained unchanged (34 ± 6%), as in control subjects.Conclusions. LV dysfunction occurs after PTCA, as described in animal models after ischemia. Alpha-blockers abolished LV, macrocirculatory and microcirculatory dysfunction, whereas the alpha-blocker effect was prevented by combining alpha- and beta-blockers. The evidence of diffuse rather than regional dysfunction, together with the opposite effects of alpha- and beta-blockade, supports the hypothesis of neural mechanisms eliciting postischemic LV dysfunction.     

Asymptomatic Left Ventricular Dysfunction

Increasingly, it is recognized that significant ventricular dysfunction can exist in the absence of symptoms for an extended period of time in patients with cardiovascular disease. Recent multicenter trials have demonstrated that therapy during the asymptomatic phase can reduce progression to symptomatic heart failure and mortality. Little is known about the epidemiology of this problem. However, preliminary studies suggest that the prevalence of asymptomatic left ventricular dysfunction may approach that of clinically apparent congestive heart failure. The mechanisms whereby some patients with severe ventricular dysfunction may remain asymptomatic while others with similar degrees of ventricular dysfunction have severe symptoms of heart failure remain unclear. By understanding these mechanisms, we may devise novel therapies which will prolong the asymptomatic phase and hopefully prevent the progression to heart failure. This review focuses on pertinent clinical and pathophysiologic issues pertaining to asymptomatic left ventricular dysfunction. This revised version was published online in July 2006 with corrections to the Cover Date.     

左心辅助装置与右心衰

左心辅助装置 (L VAD)在临床中的成功应用 ,正受到越来越多人的肯定和接受 ,在术后严重低心排的病人 ,其抢救存活率可达 5 0 % [1] ,而在终末期心泵功能衰竭等待心脏移植的病人和急性心肌炎所致的心源性休克病人其存活率更高。但一个不容忽视的问题是在应用左心辅助的病人中 ,右心衰的发生率约占 2 0 %～ 30 % [2 ,3] ,是造成病人死亡的最重要原因之一。右心衰发生的原因和机制目前还没有完全清楚 ,在如何处理上也存在一定的争论。现多数学者认为 ,左心辅助后右心衰的发生原因和机制包括 [4] :右心室原已存在的病变引起右心功能损害 ;右心…     

Left Ventricular Dysfunction in Diabetes

Patients with diabetes mellitus have a greater morbidity and mortality from cardiovascular disease than patients without diabetes. Concomitant hypertension and diabetes are associated with even greater risk of coronary disease, atherosclerotic and peripheral vascular disease, and congestive heart failure. In addition, an independent left ventricular dysfunction (diabetic cardiomyopathy) exists in patients with diabetes that may manifest itself initially as abnormalities in diastolic function but ultimately in systolic function. Firm evidence for this outcome exists experimentally, and reversal of systolic and diastolic abnormalities has been noted experimentally. The Diabetes Control and Complications Trial (DCCT) indicated that intensive glycemic control ameliorates microvascular complication of neuropathy, proteinuria, and retinopathy. Little evidence exists for macrovascular complications or for left ventricular dysfunction. Preliminary results of a canine study of glycemic control and left ventricular function are presented. Clinical correlates of this study and its results are meager. Determination of the role that glycemic control plays with regard to left ventricular systolic function and congestive heart failure awaits carefully controlled and designed clinical trials.     

Ventricular Arrhythmias and Left Ventricular Dysfunction in Familial Cardiomyopathy

ABSTRACT. In familial cardiomyopathy (CM), different forms of myocardial abnormalities including asymmetric and symmetric hypertrophy and dilated left ventricles are presented, mostly showing varying hereditary penetrance. This study presents a family with CM including three major clinical manifestations: severe ventricular arrhythmias, repolarization abnormalitites and left ventricular hypertrophy. This triad was strikingly consistent in the two generations examined. The familial pattern with an autosomal dominant inheritance did not show any linkage to the HLA region.     

心尖部心肌收缩障碍综合征

心尖部心肌收缩障碍综合征是临床上表现为一过性类似急性心肌梗死样胸痛及心电图改变,冠状动脉造影未见器质性狭窄,左心室造影心尖部收缩功能异常的一类病症。病因尚不清楚,大多在数天至数周恢复正常。     

Early Detection of Chemotherapy-Related Left Ventricular Dysfunction

Modern advances in cancer treatment have resulted in improved survival. As a result, effects of cancer therapy on other organ systems such as the heart are more likely to become clinically relevant. One such possibility is chemotherapy-related left ventricular dysfunction. Although in clinical practice cardiotoxicity is evaluated by symptoms and left ventricular ejection fraction, these occur relatively late in the disease process after the heart's compensatory mechanisms have been expended. Ideally, left ventricular dysfunction would be identified early so that cancer patients and their physicians can make informed decisions about their therapeutic options and institute careful surveillance and early initiation of cardioprotective medication where appropriate. This review discusses the role of echocardiography to detect subclinical left ventricular dysfunction in cancer patients exposed to chemotherapy with potential cardiotoxicity, particularly anthracyclines and trastuzumab.     

Left Ventricular Dysfunction in Outpatients with Frequent Ventricular Premature Complexes

Frequent ventricular premature complexes (VPCs) and VPC QRS duration are risk factors for left ventricular (LV) dysfunction. To determine which clinical characteristics and electrocardiographic features are associated with LV dysfunction (ejection fraction, <50%) and frequent VPCs, we retrospectively reviewed data from a single-center registry of all patients diagnosed with frequent VPCs at a Korean outpatient clinic.We identified 412 consecutive outpatients (mean age, 54.7 ± 16.8 yr; 227 women [55.1%]) who were diagnosed with frequent VPCs and had no structural heart disease from January 2010 through December 2017. Available transthoracic echocardiograms and 24-hour Holter monitoring data were evaluated to correlate the occurrence of VPCs and symptoms.Typical VPC-related symptoms (palpitations or dropped beats) were observed in 251 patients (61.1%). Electrocardiograms revealed VPCs with a left bundle branch block–like morphology in 327 patients (79.5%) and VPCs with an inferior axis in 353 (85.8%). Twenty-six patients (6.3%) were diagnosed with VPC-related LV dysfunction. The mean VPC burden did not differ significantly by LV functional status (11.06% ± 10.13% [normal] vs 14.41% ± 13.30% [impaired]; P=0.211). Patients with impaired LV function were more often men (P=0.027), had no typical VPC-related symptoms (P=0.006), and had significantly longer VPC QRS durations (mean, 157 ms vs 139 ms; P <0.01).Our findings suggest that male sex, absence of typical VPC-related symptoms, and a VPC QRS duration >157 ms are associated with LV dysfunction in patients with frequent VPCs, findings that may be useful in predicting such dysfunction.     

Prognosis in Patients with Left Ventricular Dysfunction and Ventricular Tachycardia Following Programmed Ventricular Stimulation

We performed programmed ventricular stimulation on 69 patients with left ventricular ejection dysfunction (ejection fraction < 50%) and clinically recognized ventricular tachycardia including 28 patients with sustained ventricular tachycardia and 41 patients with nonsustained ventricular tachycardia. An inducible arrhythmia (> 6 beats ventricular tachycardia) was found in 74% of patients. Patients with clinically sustained arrhythmias were frequently inducible (89%) with a high incidence of inducible monomorphic ventricular tachycardia (82%). Patients with clinically nonsustained ventricular tachycardia had a lower rate of inducibility (63%) including a high incidence of inducible polymorphic ventricular tachycardia (27%). Inducible patients with left ventricular dysfunction and ventricular tachycardia had a low incidence of electrophysiologically demonstrated effective drug therapy (16%). However, if an effective drug was found, the prognosis was good. Empirical drug therapy was associated with a poor prognosis in inducible and noninducible patients. Finally, an unfavorable prognosis was associated with a clinically sustained arrhythmia, a lower ejection fraction, and the presence of a left ventricular aneurysm. An inducible arrhythmia did not predict an unfavorable course. Indeed, patients with noninducible ventricular tachycardia in this group of patients were still at risk for sudden cardiac death.     

Studies of Left Ventricular Dysfunction (SOLVD)

Given the increasing incidence and dismal prognosis in congestive heart failure, it is not surprising that strenuous efforts have been made to limit the morbidity and mortality that result from this syndrome. The National Institutes of Health designed and implemented the Studies of Left Ventricular Dysfunction (SOLVD) to assess the effect of therapy with enalapril, an angiotensin-converting enzyme inhibitor, on all cause mortality in a population with left ventricular dysfunction (i.e., ejection fraction at or below 35%). Important secondary objectives included the effects of this therapy on cause-specific mortality, development of heart failure, and hospitalization for congestive heart failure. Patients within each of two arms of the trial were randomized on the basis of the administration (treatment arm) or lack (prevention arm) of concomitant therapy for congestive heart failure. The trial was double blind and placebo controlled. The mean follow-up period for the combined arms was 39.2 months, during which time there was a 16% risk reduction in all-cause mortality in the treatment arm of the trial (P equals 0.008) and an 8% risk reduction in the prevention arm (P equals NS). In the prevention arm, however, there was a 12% reduction risk for cardiovascular mortality (P equals 0.12) and a 37% reduction in risk of progression to heart failure (P is less than 0.001). Thus, the results of SOLVD indicate that therapy with an angiotensin-converting enzyme inhibitor has beneficial effects on morbidity and mortality that are apparent in a broad spectrum of patients with left ventricular dysfunction.     

Cancer Therapy-Induced Left Ventricular Dysfunction: Interventions and Prognosis

BackgroundFor multiple chemotherapeutics, cardiotoxicity is dose limiting and can lead to substantial morbidity and mortality. Early cardiac intervention has the potential to positively affect clinical course.Methods and ResultsWe reviewed 247 consecutive patients referred to the Stanford cardiology clinic for cancer therapy-associated cardiac abnormalities from 2004 to 2012. A comprehensive review of records was performed, with documentation of baseline characteristics, cardiac imaging, medications, and clinical course. Seventy-nine patients who had left ventricular ejection fraction (LVEF) declines temporally associated with cancer therapy were included. The most common malignancies were breast (46%) and hematologic (35%); 71% of the patients were female, and overall mean age was 52 years. The primary cancer therapeutics associated with LVEF decline included anthracyclines, trastuzumab, and tyrosine kinase inhibitors. The mean LVEF was 60% before cancer therapy and 40% after cancer therapy. The most common cardiac interventions included beta-blockers (84%) and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (83%). Mean LVEF after cardiac intervention rose to 53%; 77% of patients had LVEF recovery to ≥50%, and 68% of these patients had recovery within 6 months of starting cardiac therapy; 76% of patients were able to continue their planned cancer therapy.ConclusionsWith appropriate cardiac intervention, the majority of patients with LVEF decline from cancer therapy can achieve LVEF recovery and complete their cancer therapy.     

Left Ventricular Dysfunction and Heart Failure Mechanistic and Therapeutic Distinctions

Dysfunction of the left ventricle may result from a variety of insults, all of which may initiate a self-perpetuating process of ventricular remodeling which may progress to end-stage heart disease. Symptoms of heart failure may or may not coexist with this ventricular remodeling. Treatment and prevention of these two largely distinct entities differ. Symptoms may respond to diuretics, vasodilators and digoxin. Progressive ventricular remodeling may be slowed by angiotensin converting enzyme inhibitors, hydralazine + isosorbide dinitrate and beta blockers. Prevention of symptomatic heart failure is dependent on early recognition of ventricular dysfunction and aggressive treatment to slow its progression. Development of more effective and targeted therapies will be dependent on expanded insight into the cellular and molecular mechanisms contributing to the remodeling process.     

Apparent Acute Reversible Right Ventricular Pacing‐Induced Left Ventricular Dysfunction

Apparent Acute Reversible Right Ventricular Pacing‐Induced Left Ventricular Dysfunction . We report the case of a 70‐year‐old Caucasian male with a dual chamber (right atrium/right ventricle) pacemaker implanted for sinus node dysfunction and not pacemaker (PM) dependent who was found to have an apparent acute worsening of left ventricular (LV) function with right ventricular (RV) apical pacing caused by the mode switch to VVI pacing as battery depletion occurred. LV dysfunction resolved immediately with RV pacing turned off. To our knowledge, this is the first report of this phenomenon. (J Cardiovasc Electrophysiol, Vol. 24, pp. 224‐226, February 2013)     

超声观察原发性高血压患者左室肥厚与冠脉内皮功能障碍的关系

目的探讨原发性高血压(EH)左室肥厚(LVH)与冠脉内皮功能障碍之间的关系。方法超声观察34例EH患者和15例正常人的心脏结构及功能,此后研究受检者含服硝酸甘油所致的血管非内皮依赖性扩张性(DING),并结合冷加压超声心动图试验评价其冠状动脉内皮依赖性扩张性(DICPT)。结果与正常组(14.98%±1.54%)相比,非LVH(15/34)和LVH(19/34)患者的冠状动脉内皮依赖性扩张性(9.18%±1.12%;4.27%±2.01%)均显著减小,且后者较前者更甚(P<0.001)。LVH组患者的左室重量指数(LVMI)(159.6±29.6)g/m2较非LVH组(98.8±12.8)g/m2及正常组(113.1±13.1)g/m2增大(P<0.001)。LVH组、非LVH组的血压均较正常组增高,但前两组间的血压无显著性差异。3组间的冠脉非内皮依赖性扩张性、EF、FS及年龄、血脂、血糖等无显著性差异(P>0.05)。相关分析显示:患者的左室重量指数与冠状动脉内皮依赖性扩张性呈良好负相关(r=-0.54,P<0.0001)。结论原发性高血压患者左室肥厚与冠脉血管内皮功能障碍密切相关,后者可能在左室肥厚的发生发展过程起作用。     

超声观察原发性高血压患者左室肥厚与冠脉内皮功能障碍的关系

目的探讨原发性高血压(EH)左室肥厚(LVH)与冠脉内皮功能障碍之间的关系.方法超声观察34例EH患者和15例正常人的心脏结构及功能,此后研究受检者含服硝酸甘油所致的血管非内皮依赖性扩张性(DING),并结合冷加压超声心动图试验评价其冠状动脉内皮依赖性扩张性(DICPT).结果与正常组(14.98%±1.54%)相比,非LVH(15/34)和LVH(19/34)患者的冠状动脉内皮依赖性扩张性(9.18%±1.12%;4.27%±2.01%)均显著减小,且后者较前者更甚(P＜0.001).LVH组患者的左室重量指数(LVMI)(159.6±29.6)g/m2较非LVH组(98.8±12.8)g/m2及正常组(113.1±13.1)g/m2增大(P＜0.001).LVH组、非LVH组的血压均较正常组增高,但前两组间的血压无显著性差异.3组间的冠脉非内皮依赖性扩张性、EF、FS及年龄、血脂、血糖等无显著性差异(P＞0.05).相关分析显示患者的左室重量指数与冠状动脉内皮依赖性扩张性呈良好负相关(r=-0.54,P＜0.000 1).结论原发性高血压患者左室肥厚与冠脉血管内皮功能障碍密切相关,后者可能在左室肥厚的发生发展过程起作用.