Setting Of Left Ventricular Dysfunction Research Articles

Abstract 17504: Revisiting the Etiology of a Non-Ischemic Cardiomyopathy

Introduction: In the era of REVIVED-BCIS2 and ISCHEMIA clinical trials, the role of routine invasive coronary angiography for treatment of coronary artery disease (CAD) in the setting of left ventricular dysfunction has come into question. While the majority of heart failure (HF) patients undergo some form of non-invasive ischemic evaluation, there are a wide range of opinions on which testing modality is the most appropriate. Case: This is a 53 year-old man with a history of HTN, HLD, and presumed non-ischemic cardiomyopathy and LVEF of 15-20%, first diagnosed in 2009. He had a family hx of heart disease in several distant relatives, thus the etiology was presumed familial. In 2022, he had NYHA class II symptoms and a routine echo showed a LVEF of 25% with anteroseptal hypokinesis. Given these findings, a coronary CTA was obtained. This demonstrated infarct in the LAD territory and a proximal left main to mid-LAD aneurysm measuring up to 7 mm with a partially calcified shell and peripheral thrombus, consistent with prior Kawasaki’s disease (KD). He was initiated on a DOAC to prevent further embolic events and aspirin. He is now undergoing serial monitoring of the aneurysm size, thrombus burden, and functional testing to monitor for ischemia. Discussion: Non-invasive anatomic testing to evaluate for CAD in HF patients can provide useful information over a functional assessment. KD is a rare disease with an estimated incidence rate of ≈25 per 100,000 children less than 5 years of age. KD can lead to coronary artery aneurysms, which often contain thrombi, and subacute/chronic myocarditis. The affected arteries can become stenotic over time or even occlude, leading to ischemic injury later in life. Early recognition of this rare disease is important to initiate appropriate treatment and prevent thromboembolic complications. Conclusion: KD is a rare cause of adult cardiomyopathy. Anatomic testing was essential to appropriately diagnose and treat this patient’s cardiomyopathy.

Hybrid and parallel extracorporeal membrane oxygenation circuits

Hybrid and parallel extracorporeal membrane oxygenation circuits

Trastuzumab-Induced Cardiomyopathy.

Trastuzumab targets the human epidermal growth factor receptor 2 (HER2). Its overexpression occurs in 25% of breast cancers and is associated with aggressive tumor characteristics and poor prognosis in absence of targeted therapy. Trastuzumab dramatically improves HER2-positive breast cancer outcomes; however, its clinical use is associated with left ventricular dysfunction and heart failure. Patients receiving trastuzumab or other HER2-targeted therapies undergo routine cardiac function assessment. Holding and/or stopping trastuzumab treatment in the setting of left ventricular dysfunction is recommended. This article summarizes the role of trastuzumab in cancer treatment, the mechanisms of trastuzumab-induced cardiotoxicity, recent clinical investigations, and current controversies.

Revascularization in Cardiogenic Shock and Advanced Heart Failure.

Ischemic heart disease is the most common cause of heart failure with systolic dysfunction. The progressive course of heart failure characterized by increasing levels of care and worsening quality of life often indicates an advanced stage. Similarly, cardiogenic shock remains a major clinical problem with prohibitively high mortality rates despite major advances in clinical care. Here, we review the current treatment options and available data for revascularization in patients with ischemic cardiomyopathy, advanced heart failure, and cardiogenic shock. We also explore the emerging role of Interventional Heart Failure specialist within the Heart Team. Although guideline-directed medical therapy remains the cornerstone treatment strategy for patients with advanced heart failure, coronary revascularization is sometimes indicated. There is a relatively paucity of evidence regarding different revascularization strategies and the use of acute mechanical circulatory support in patients with advanced heart failure and in those presenting with cardiogenic shock. A deep understating of the physiologic and hemodynamic effects of different acute mechanical support platforms is of paramount importance in preparation for revascularization in these patients. The decision regarding revascularization in patients with coronary artery disease in the setting of left ventricular dysfunction remains challenging. Clinical decision-making in these cases requires interdisciplinary discussion and assessment of the potential long-term survival derived from surgical revascularization against its higher perioperative risk.

The Importance of Assessing Arteriovenous Fistula Patency in the Setting of Persistent Pulmonary Hypertension After Combined Liver Kidney Transplant

Introduction: Portopulmonary hypertension (PoPH) is a well-documented vascular complication in patients with end-stage liver disease. In the setting of left ventricular dysfunction, patients with cirrhosis and ESRD can develop pulmonary venous hypertension. The hemodynamic effects of arteriovenous fistulas (AVFs) in patients with both cirrhosis and ESRD in exacerbating pulmonary arterial and venous hypertension are rarely reported in the literature. A 54-year-old male with a history of 2 renal transplants and a liver transplant for cirrhosis presented with several weeks of progressive dyspnea, orthopnea, and lower extremity edema. His first renal allograft failed due to chronic rejection, requiring him to resume hemodialysis in 2002 through a left upper extremity AVF. He began having recurrent ascites in 2008 and was referred for evaluation of possible liver kidney transplant. His echocardiogram showed an elevated right ventricular systolic pressure of 74.8 mmHg. Subsequent right heart catheterization (RHC) was consistent with pulmonary arterial hypertension, with mean pulmonary arterial pressure (mPAP) 41 mmHg, pulmonary vascular resistance (PVR) 254 dyne*sec/cm5, and cardiac index (CI) 4 dyne*sec/cm5. After 6 months of therapy with sildenafil, his mPAP decreased to 28 mmHg, allowing him to successfully undergo a simultaneous liver kidney transplant in 2009. The patient did well until 3 years later, when he presented with volume overload. Repeat echocardiogram revealed a preserved ejection fraction and a mPAP of 81.6 mmHg. The patent’s RHC revealed a relatively normal PCWP and elevated transpulmonary gradient (TPG) concerning for worsening pulmonary hypertension (mPAP 55 mmHg, PVR 343 dyne*sec/cm5). His symptoms progressed despite receiving aggressive diuresis and ICU support for right ventricular syndrome. Based on the patient’s high cardiac output and pulmonary hypertension with normal PVR, the diagnosis of high output heart failure was made. The patient’s AVF was ligated out of clinical concern for high output through the patient’s fistula causing exacerbation of pulmonary arterial and venous hypertension. Repeat RHC showed decrease in mPAP to 36.6 mmHg 7 months after AVF ligation, consistent with continued improvement of respiratory symptoms with stable liver and kidney allograft function. This case illustrates the potential importance of evaluating graft patency in patients with pre-existing PoPH, given the risk of developing high output heart failure. Given the probability that an AVF will remain patient after renal transplant, clinicians should carefully consider assessing AVF patency and flow in the setting of worsening clinical signs and symptoms suggestive of high-output heart failure.

Influence of Age-Related Versus Non–Age-Related Renal Dysfunction on Survival in Patients With Left Ventricular Dysfunction

Normal aging results in a predictable decrease in glomerular filtration rate (GFR), and low GFR is associated with worsened survival. If this survival disadvantage is directly caused by the low GFR, as opposed to the disease causing the low GFR, the risk should be similar regardless of the underlying mechanism. Our objective was to determine if age-related decreases in estimated GFR (eGFR) carry the same prognostic importance as disease-attributable losses in patients with ventricular dysfunction. We analyzed the Studies Of Left Ventricular Dysfunction limited data set (n = 6,337). The primary analysis focused on determining if the eGFR-mortality relation differed by the extent to which the eGFR was consistent with normal aging. Mean eGFR was 65.7 ml/min/1.73 m(2) (SD = 19.0). Across the range of age in the population (27 to 80 years), baseline eGFR decreased by 0.67 ml/min/1.73 m(2)/year (95% confidence interval [CI] 0.63 to 0.71). The risk of death associated with eGFR was strongly modified by the degree to which the low eGFR could be explained by aging (p for interaction <0.0001). For example, in a model incorporating the interaction, uncorrected eGFR was no longer significantly related to mortality (adjusted hazard ratio 1.0 per 10 ml/min/1.73 m(2), 95% CI 0.97 to 1.1, p = 0.53), whereas a disease-attributable decrease in eGFR above the median carried significant risk (adjusted hazard ratio 2.8, 95% CI 1.6 to 4.7, p <0.001). In conclusion, in the setting of left ventricular dysfunction, renal dysfunction attributable to normal aging had a limited risk for mortality, suggesting that the mechanism underlying renal dysfunction is critical in determining prognosis.

Chronic Heart Failure

Heart Failure is a progressive clinical syndrome marked by venous congestion and maladaptive neurohormonal activation in the setting of left ventricular dysfunction. More recently, another face of this syndrome is beginning to emerge involving metabolic derangements implicating other organs - adipose tissue, skeletal muscle - and the endocrine systems (leptin, adiponectin, insulin and insulin-like growth factor) regulating their mass and function. The metabolic abnormalities which have been described thus far include: 1. Systemic and myocardial insulin resistance (IR); 2. Mitochondrial dysfunction; 3. Progressive weight loss leading to cachexia in the more advanced stages; and 4. Myocardial energetic failure associated with a down-regulation of fatty acid uptake and oxidation resulting in a rigid shift from fatty acid to glucose as the primary energy source for maintenance of ATP flux in the heart - a preferential switch to a fetal-like gene program regulating cardiac energetics. Despite the important advances to date, our understanding of all the components comprising the metabolic phenotype of human heart failure is certainly incomplete, if not rudimentary. (SELECT FULL TEXT TO CONTINUE)

Sympathetically Mediated Changes in Capacitance

“To be accepted as a paradigm, a theory must seem better than its competitors, but it need not, and in fact never does, explain all the facts with which it can be confronted.” Thomas Kuhn, The Structure of Scientific Revolutions ### Heard on Rounds “A 57-year-old patient with a history of heart failure states that she began experiencing worsening shortness of breath 4 days prior to admission, with lower extremity edema developing 1 day prior to admission. She is compliant with her medications, though has had similar admissions previously. She states that her weight at home increased by “a couple of pounds” 2 days ago and that she increased her diuretic dose but her symptoms worsened. She says that she generally adheres to her low salt diet, but admits to eating pretzels 5 days ago. The physical examination showed BP 136/84, HR 94, weight 3 lbs above baseline, elevated JVP, basilar rales, and 1+ pedal edema.” As the intern finishes the presentation, the Senior expresses surprise that the patient's weight had increased only 3 pounds, and comments about salt and volume overload leading to acute decompensated heart failure (ADHF). The Attending adds that recent data reveal that many patients presenting with ADHF have minimal or no weight gain, but that there is no clear mechanism to explain this phenomenon. They set in place plans for diuresis, increasing vasodilators, and further patient education. On the surface, there is nothing remarkable about this case, and the usual approaches to treat this entity have remained remarkably consistent since the advent of loop diuretics over 50 years ago: salt restriction, patient education, uptitration of medications if not already at optimal doses, and diuresis. However, approximately 1 in 4 such patients are readmitted to the hospital within 30 days,1 and the disease continues to progress. It is clear …

Pathophysiologie der chronischen Herzinsuffizienz

Heart failure is a progressive and often fatal disease process. In general, the pathophysiologic mechanisms responsible for progressive myocyte dysfunction and cell loss, cardiac remodeling and arrhythmias involve signaling mechanisms that alter myocardial gene expression. These changes in gene expression are complex and involve contractile proteins, ion channels, Ca(++) handling, apoptosis, cell metabolism, the extracellular matrix, signal transduction pathways and growth factors. In the failing heart, several changes occur in cardiac adrenergic receptor-signal transduction pathways. The most striking of these changes occur in beta-adrenergic receptors, and of the changes in beta-adrenergic receptors beta1-receptor down-regulation is the most prominent. Other changes include uncoupling of beta2-adrenergic receptors and increased activity of the inhibitory G-protein. Most of these changes appear to be related to increased activity of the adrenergic nervous system, i.e. increased exposure to norepinephrine. Antagonists of the adrenergic nervous system may improve left ventricular function and outcome in patients with heart failure. This fact supports the notion that activation of these neurohormonal systems exerts a net long-term detrimental effect on the natural history of chronic heart failure and that myocardial adrenergic desensitization phenomena are at least partially maladaptive in the setting of left ventricular dysfunction. In addition to functional alterations structural remodeling plays a major role in the progression of various heart diseases to congestive heart failure. Major contributors to this remodeling process in the heart include alterations in myocyte shape, myocyte number and extracellular matrix. However, it is unclear as to which of these changes is most critical in the development of congestive heart failure, and this may vary by etiology.

Neurogenic Cardiac Injury.

Cardiac injury may occur following many types of brain injury, although the most widely investigated form of neurocardiogenic injury is subarachnoid hemorrhage (SAH). Echocardiography may help prognosticate and aid in the treatment of SAH if left ventricular (LV) dysfunction is suspected or if troponin levels are elevated. Cardiac catheterization, however, is not routinely recommended in SAH patients with LV dysfunction and elevated troponin. The priority should be treatment of the underlying neurological condition, even in the setting of LV dysfunction. Cardiac injury that occurs following an SAH appears to be reversible. For patients that develop brain death cardiac evaluation under optimal conditions may help increase the donor pool.

Prognostic value of baseline electrophysiology studies in patients with sustained ventricular tachyarrhythmia: The Antiarrhythmics Versus Implantable Defibrillators (AVID) trial

Objectives We sought to determine the value of electrophysiology (EP) testing in patients with ventricular fibrillation (VF), ventricular tachycardia (VT) with syncope, or sustained VT in the setting of left ventricular dysfunction. Background Traditionally, EP testing is part of the workup of patients with sustained VT or VF. Recently, some have suggested that EP testing is unnecessary in these patients, many of whom are likely to receive an implantable cardioverter-defibrillator (ICD). Methods Within a multicenter trial (Antiarrhythmics Versus Implantable Defibrillators) designed to evaluate whether drugs or ICD resulted in a better outcome, data were analyzed regarding EP testing. Although this testing was not required, it was performed in >50% of patients. Information regarding the results of EP testing was correlated to baseline clinical characteristics and outcome. Results Of 572 patients subjected to an EP test, 384 (67%) had inducible sustained VT or VF. Inducible patients were more likely to have coronary artery disease, previous infarction, and VT as their index arrhythmic event. Inducibility of VT or VF did not predict death or recurrent VT or VF. Conclusions Information derived from EP testing in this patient population, particularly those with VF, is of limited value and may not be worth the risks and costs of the procedure, particularly in those patients likely to receive an ICD. (Am Heart J 2002;144:478-84.)

Echocardiographic ischemia is a predictor of death in patients after bypass surgery in the setting of left ventricular dysfunction

Echocardiographic ischemia is a predictor of death in patients after bypass surgery in the setting of left ventricular dysfunction

Biphasic and monophasic transthoracic defibrillation in pigs with acute left ventricular dysfunction

Objective: Our purpose was to compare biphasic versus monophasic shock success for VF termination in a porcine model of acute left ventricular (LV) dysfunction. Background: For the termination of ventricular fibrillation (VF), transthoracic biphasic waveform shocks achieve higher success rates than monophasic shocks. However, the effectiveness of biphasic versus monophasic defibrillation in a setting of left ventricular dysfunction has not been reported. Methods: In 23 open-chest adult swine (15–25 kg), LV dysfunction [≥25% decline in cardiac output (CO)] was induced by continuous inhalation of halothane (1–1.75%). Each pig randomly received transthoracic biphasic and monophasic shocks at three energy levels (30, 50 and 100 J) in two conditions: baseline and LV dysfunction. Halothane effect on left ventricular size and contraction was measured by echocardiography in three additional swine. Results: With halothane, pigs demonstrated a decline in CO (baseline 4.16±0.19, halothane 2.72±0.19 l/min, P<0.01), mean arterial pressure (baseline 107.2±3.5, halothane 80.1±3.4 mmHg, P<0.01) and increased left ventricular end-diastolic pressure (baseline 6.4±0.9, halothane 12.7±0.8 mmHg, P<0.01). LV diameters increased and fractional shortening fell. During baseline, biphasic shocks achieved significantly greater success (termination of VF) compared to monophasic waveforms (100 J: biphasic 83.3±9.5 versus monophasic 38.9±9.5%, P<0.01; 50 J: biphasic 67.1±8.8 versus monophasic 11.8±5.7%, P<0.01; 30 J: biphasic: 31.9±6.4 versus monophasic 0±0%, P<0.01). The superiority of the biphasic waveform to terminate VF was retained during LV dysfunction at all energy levels (100 J: biphasic 78.3±7.3 versus monophasic 37.5±8.1%, P<0.01; 50 J: biphasic 65.5±11.5 versus monophasic 11.7±5.9%, P<0.01; 30 J: biphasic: 40.6±8.0 versus monophasic 3.1±3.1%, P<0.01). Within both waveforms, there were no significant differences in percent shock success at any energy level comparing baseline with LV dysfunction. Conclusion: In this porcine model of acute LV dysfunction, biphasic waveform shocks were not only superior to monophasic waveform shocks for termination of VF during baseline, but retained superiority to monophasic waveform shocks when LV dysfunction was present.

Right Ventricular Infarction.

Right ventricular (RV) ischemia occurs in a substantial proportion of patients with acute inferior myocardial infarction (MI), and may result in severe hemodynamic compromise. This defines a high-risk subset of patients with a mortality rate of 25% to 30%, as opposed to an overall mortality rate of approximately 6% patients with inferior MI without right ventricular infarction (RVI). Early recognition of RV ischemic dysfunction is of great importance in inferior MI with clinical evidence of low cardiac output, because the therapeutic approaches are very different from that for cardiogenic shock resulting predominantly from severe left ventricular (LV) failure. Management of RV ischemic dysfunction includes maintenance of RV preload with volume loading and maintenance of atrioventricular synchrony, inotropic support, and reduction of RV afterload in the setting of LV dysfunction. Reperfusion therapy should be initiated in patients with RV ischemic dysfunction. Though the RV appears to be relatively resistant to infarction and has a remarkable ability to recover even after prolonged occlusion, successful reperfusion of the right coronary artery and major RV branches rapidly improves RV ejection fraction and hemodynamic status, and decreases in-hospital mortality and morbidity.

Cardiac surgery: postoperative arrhythmias.

Arrhythmias are common after surgery, particularly after cardiac surgery. Atrial fibrillation is the most common arrhythmia encountered postoperatively, although ventricular arrhythmias and conduction disturbances can also occur. Older age is the most consistent predictor of postoperative atrial arrhythmias. beta-adrenergic blockers, amiodarone, and sotalol are the most effective at preventing postoperative atrial fibrillation. Sustained ventricular arrhythmias in the recovery period after cardiac surgery warrant aggressive therapy, usually with an implantable cardioverter-defibrillator in the absence of reversible causes. Postoperative, nonsustained ventricular tachycardia in the setting of left ventricular dysfunction and ischemic coronary disease also usually warrants risk stratification and possible treatment, often with electrophysiologic testing and implantation of an implantable cardioverter-defibrillator, if sustained ventricular arrhythmias are induced. Transient bradyarrhythmias may be managed with temporary pacing wires placed at surgery, but significant and persistent atrioventricular block or sinus node dysfunction can occur and indicate a need for permanent pacing.

Alterations in adrenergic receptor signaling in heart failure.

In the failing heart, several changes occur in cardiac adrenergic receptor-signal transduction pathways. The most striking of these changes occur in beta-ARs, and of the changes in beta-adrenergic receptors, beta1-receptor down-regulation is the most prominent. Other changes include uncoupling of beta2-adrenergic receptors and increased activity of the inhibitory G-protein, Gi. Most of these changes appear to be related to increased activity of the adrenergic nervous system, i.e. increased exposure to norepinephrine. Antagonists of the adrenergic nervous system improve left ventricular function and outcome in patients with heart failure. This fact supports the notion that activation of these neurohormonal systems exerts a net long-term detrimental effect on the natural history of chronic heart failure and that myocardial adrenergic desensitization phenomena are at least partially adaptive in the setting of left ventricular dysfunction.

Intravenous Amiodarone for Arrhythmia Management

Letters15 March 1998Intravenous Amiodarone for Arrhythmia ManagementRuey J. Sung, MDRuey J. Sung, MDStanford University Medical Center; Stanford, CA 94305Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-6-199803150-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We thank Drs. Halkin and Shibolet for pointing out our editing error. On line four of the last paragraph in the left column on page 297, references 36 and 43 should have been cited in addition to 34.With regard to the issue of considering intravenous amiodarone as the first-line agent for cardioversion for a recent onset of atrial fibrillation or flutter, we strongly believe that the choice of agent should be individualized according to the clinical setting. In the setting of left ventricular dysfunction or acute myocardial infarction, we agree that intravenous amiodarone could be considered a ... Author, Article, and Disclosure InformationAffiliations: Stanford University Medical Center; Stanford, CA 94305 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 March 1998Volume 128, Issue 6Page: 505KeywordsAcute myocardial infarctionArrhythmiaAtrial fibrillationDrugs Issue Published: 15 March 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...

Isoflurane, but not halothane, improves indices of diastolic performance in dogs with rapid ventricular, pacing-induced cardiomyopathy.

The left ventricular (LV) mechanical effects of isoflurane and halothane were examined in dogs with rapid LV pacing-induced cardiomyopathy. These experiments tested the hypothesis that isoflurane and halothane differentially enhance indices of diastolic performance in dogs with moderate LV dysfunction. Eight dogs were chronically instrumented for measurement of LV and aortic pressures, subendocardial segment length, and cardiac output. Contractility was quantified by preload recruitable stroke work (Mw). Diastolic function was evaluated with a time constant of isovolumic relaxation (tau), segment lengthening velocities and time-velocity integrals during early filling (dL/dtE and TVI-E) and atrial systole (dL/dtA and TVI-A), and a regional chamber stiffness constant (Kp). Hemodynamics and LV function were recorded in the conscious state before pacing. The left ventricles of the dogs were then continuously paced at ventricular rates between 220 and 240 beats.min-1 for 10 +/- 1 days and monitored on a daily basis. After the development of moderate LV dysfunction, pacing was temporarily discontinued, and dogs were studied in sinus rhythm in the conscious state and after 20 min equilibration at 1.1, 1.4, and 1.7 minimum alveolar concentration isoflurane and halothane on separate days. Chronic rapid pacing increased baseline (sinus rhythm) heart rate, LV end-diastolic pressure, and end-diastolic segment length and decreased mean arterial pressure, LV systolic pressure, and cardiac output. Mw decreased and tau and Kp increased, consistent with LV systolic and diastolic dysfunction. Reductions in dL/dtE/dL/dtA and TVI-E/A occurred, which indicated that LV filling was more dependent on atrial systole. In dogs with cardiomyopathy, isoflurane and halothane increased heart rate and decreased mean arterial pressure, LV systolic pressure, LV end-diastolic pressure, cardiac output, Mw, and Kp. Decreases in LV end-diastolic pressure were more pronounced in dogs anesthetized with 1.1 minimum alveolar concentration isoflurane compared with halothane. Halothane-induced decreases Mw were greater than those observed with equi-minimum alveolar concentration isoflurane. A reduction in tau and increases in TVI-E/TVI-A and the ratio of early to total LV filling were observed with isoflurane. In contrast, halothane caused dose-related reductions in dL/dtE, dL/dtA, TVI-E, and TVI-A, and did not improve the ratios of these variables. Isoflurane, but not halothane, improved several indices of diastolic performance in dogs with pacing-induced LV dysfunction, despite producing simultaneous negative inotropic effects. These findings can probably be attributed to favorable reductions in LV preload and not to direct lusitropic effects. Improvement of filling dynamics may partially offset the decrement in LV systolic function by isoflurane in the setting of LV dysfunction.

Low-dose amiodarone for atrial fibrillation

Concerns about proarrhythmia risk and inefficacy associated with class I antiarrhythmic drugs have revived interest in low-dose amiodarone (maintenance dose 200–400 mg/day) for suppression of atrial fibrillation. In nonrandomized trials of amiodarone for atrial fibrillation refractory to conventional agents, amiodarone has been successful in maintaining sinus rhythm in 53–79% of patients during a mean follow-up of 15–27 months. Intolerable side effects, including pulmonary toxicity, are in the range of 1–12% per year and resolve following amiodarone withdrawal in the majority of cases. Proarrhythmia risk associated with amiodarone, even in the setting of left ventricular dysfunction, is extremely low. In patients with congestive heart failure, in whom other pharmacologic options are limited by proarrhythmia risk and negative inotropism, preliminary experience with amiodarone is especially promising. Randomized trials are needed, directly comparing amiodarone to conventional antiarrhythmic therapy for atrial fibrillation suppression and comparing amiodarone to warfarin for thromboembolism prevention in patients with atrial fibrillation refractory to conventional antiarrhythmic drugs.

Effectiveness of captopril in reversing renal vasoconstriction after Q-wave acute myocardial infarction

The purpose of this investigation was to study whether favorable renal effects might contribute to the influence of captopril in offsetting ventricular dilatation after infarction. Effective renal plasma flow and glomerular filtration rate were estimated by isotope injection methods in 20 patients on days 2, 7, 8, 42 and 180 after a first transmural anterior myocardial infarction. After measurements on day 7, patients were randomized to receive either captopril 25 mg 3 times daily (n = 10) or placebo (n = 10) for the remainder of the study. At baseline (day 7) there were no differences between the 2 treatment groups in radionudide left ventricular ejection fraction, effective renal plasma flow, glomerular filtration rate or neurohormones. Left ventricular ejection fractions (40 ± 4% [mean ± 2 SD] at baseline) were higher in the captopril- than the placebo-treated patients on days 42 (p < 0.05) and 180 (p < 0.01) after infarction. Effective renal plasma flow became significantly higher at all time points after randomization in the captopril-treated group than in the placebo group (p < 0.001). A similar but lesser trend was observed for glomerular filtration rate. Plasma atrial natriuretic factor and aldosterone were significantly higher in the placebo group (p < 0.05). Renal hemodynamic indexes were directly correlated with and neurohumoral indexes inversely correlated with ejection fractions. In a second group of 12 patients with higher baseline ejection fractions (48 ± 4%) after an inferior infarction, none of these beneficial effects of captopril were demonstrable. It is proposed that in the setting of left ventricular dysfunction after infarction, a prompt and sustained improvement in renal hemodynamics, by reducing inappropriate fluid retention and thus ventricular preload, may be one contributory mechanism by which captopril prevents progression of left ventricular dilatation.