SEARCH · Search PubMed

Results for “ventricular dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

PubMed1990

Hemodynamic profile of amiodarone during acute and long-term administration in patients with ventricular dysfunction.

One of the potential adverse effects of anti-arrhythmic agents is an impairment of cardiac function as a result of their intrinsic negative inotropic properties. Amiodarone, in animals, also induces dose-related negative inotropic effects, in addition to coronary and systemic vasodilatation and slowing of the heart. Likewise, in most human studies, intravenous amiodarone gives rise to early systemic and coronary vasodilatation, followed by a reduction in contractility. Depending on the relative impact of these opposing effects on the left ventricle, the changes in heart rate, cardiac output and left ventricular filling pressure are variable. Particularly in patients with pre-existing ventricular dysfunction, cardiac pump function is impaired further when relatively high dosages of amiodarone are used without its solvent Tween 80. In contrast, fast bolus administrations, eg. 5 mg/kg amiodarone in 5 minutes, result in an improvement of cardiac output, albeit at the expense of an increase in left ventricular filling pressure. The latter observation suggests that intravenous amiodarone should be given with caution in patients with heart failure and elevated left ventricular filling pressures. When given by mouth, amiodarone does not have significant hemodynamic effects, other than a moderate reduction in heart rate and, occasionally, in diastolic blood pressure. Cardiac pump function is not affected, even in patients with ventricular dysfunction or heart failure, in whom chronic oral administration of the drug is well tolerated.

Amiodarone↗

PubMed1991

Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition.

Left ventricular dysfunction can be improved with angiotensin-converting-enzyme inhibition started 1 week after myocardial infarction or later. To see whether earlier intervention may confer greater benefit, a double-blind study was carried out in which 100 patients with Q wave myocardial infarction, but without clinical heart failure, were randomly allocated treatment with captopril 50 mg twice daily or placebo starting 24-48 h after onset of symptoms. Left ventricular volumes were measured regularly during 3 months of treatment and after a 48 h withdrawal period by means of two-dimensional echocardiography. The placebo group showed significant increases in left ventricular end-diastolic (LVEDVI) and end-systolic (LVESVI) volume indices, with the ejection fraction unchanged. By contrast, the captopril group showed a slight but not significant rise in LVEDVI and a significant reduction in LVESVI with ejection fraction increased significantly. At 3 months there was a 4.6% difference in the change in ejection fraction from baseline between the groups (p less than 0.0001). Most of the treatment benefit was evident at 1 month and there were no changes in left ventricular volumes after 48 h withdrawal of treatment at 3 months. Heart failure requiring treatment with frusemide developed in 7 patients in each group during the study period; 3 of these (1 captopril-treated, 2 placebo-treated) had to be withdrawn from the trial with severe heart failure requiring open treatment. Thus early treatment with captopril is effective in preventing the ventricular dilatation that can occur after Q wave myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1996

Left ventricular dysfunction due to the new ischemic outcomes: stunning and hibernation.

Several potential manifestations and outcomes are associated with myocardial ischemia and reperfusion. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When ischemia is less severe or shorter in duration, recovery of contraction may occur instantaneously or more commonly, after considerable delay, which is the condition recognized as "stunned myocardium." Stunning is defined as a transient left ventricular dysfunction that persists after reperfusion despite the absence of irreversible damage and restoration of normal or near-normal coronary flow. Oxidative stress and alteration of calcium homeostasis during reperfusion are the probable causes of stunning. Clinically, stunning may occur after acute infarction, successful thrombolysis, unstable angina, angioplasty, resolution of coronary spasm, open-heart surgery, or transplantation. It can be treated with interventions aimed at prevention or reversal. When ischemia is prolonged but less severe, myocytes may remain viable but exhibit depressed contraction. Under these conditions, reperfusion restores normal contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed "hibernating myocardium." The intrinsic mechanisms of this condition are unknown. Clinically, it is very important to diagnose hibernation because reperfusion of the hibernating myocardium by angioplasty or heart surgery restores contraction, and this correlates with long-term survival. A number of methods are available to access the hibernating myocardium. These include cardiac imaging techniques that evaluate myocardial viability, such as positron emission tomography and thallium myocardial imaging, or methods that evaluate contractile reserve, such as low-dose dobutamine echocardiography. Interestingly, reperfusion of patients with end-stage ischemic cardiomyopathy and hibernating myocardium can be considered an alternative to transplantation.

Cardiomyopathies↗

PubMed2004

Coronary artery bypass grafting alone for advanced ischemic left ventricular dysfunction with significant mitral regurgitation: early and midterm outcomes in a small series.

In 31 consecutive patients with ischemic left ventricular dysfunction and mitral regurgitation ranging from 2/4 to 3/4 (mean, 2.87 +/- 0.34), we performed coronary bypass grafting alone and assessed early and midterm outcomes. Our patients' mean preoperative New York Heart Association functional class was 3.64 +/- 0.48, and their mean left ventricular ejection fraction was 0.25 +/- 0.05. Preoperative thallium imaging revealed that all patients had at minimum a partially reversible defect in the anterior wall. All patients survived the operation. Hospital length of stay ranged from 5 to 21 days (mean, 8.35 +/- 4.07 days), and mean length of follow-up was 21.35 +/- 13.24 months. Postoperatively, patients' functional classification improved to a mean of 1.32 +/- 0.6; left ventricular ejection fraction improved to a mean of 0.43 +/- 0.09; and severity of mitral regurgitation decreased to a mean of 1.35 +/- 0.96. Statistical analysis showed that all improvements were significant. Five late cardiac deaths occurred. Preoperative variables showed no correlation with late death. However, postoperative left ventricular ejection fraction and mitral regurgitation did correlate with late death, which suggests that the reversibility of damaged ischemic myocardium plays an important role after revascularization. This study supports the concept that ischemic mitral regurgitation might well improve after myocardial revascularization regardless of its severity; therefore, it should not be corrected at the primary operation, except in patients with organic valvular changes.

Adult↗

PubMed1998

Contrast magnetic resonance imaging in the assessment of myocardial viability in patients with stable coronary artery disease and left ventricular dysfunction.

BACKGROUND: The utility of contrast MRI for assessing myocardial viability in stable coronary artery disease (CAD) with left ventricular dysfunction is uncertain. We therefore performed cine and contrast MRI in 24 stable patients with CAD and regional contractile abnormalities and compared MRI findings with rest-redistribution 201Tl imaging and dobutamine echocardiography. METHODS AND RESULTS: Delayed MRI contrast enhancement patterns were examined from 3 to 15 minutes after injection of 0.1 mmol/kg IV gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA). Comparable MRI and 201Tl basal and midventricular short-axis images were subdivided into 6 segments. Segments judged nonviable by quantitative and qualitative assessment of 201Tl scans showed persistent, systematically greater MRI contrast signal intensity than segments judged viable (P</=0.002). Delayed contrast hyperenhancement also occurred in segments judged nonviable by dobutamine echocardiography (P</=0.03). The presence or absence of hyperenhancement correlated most closely with nonviability and viability, respectively, in segments that were akinetic or dyskinetic under resting conditions (83% concordance with 201Tl in both cases). In segments with resting hypokinesis, 58% of segments showing hyperenhancement were judged viable by 201Tl and may have represented an admixture of scar tissue and viable myocardium. CONCLUSIONS: Delayed (by 3 to 15 minutes) hyperenhancement of Gd-DTPA contrast-enhanced MRI images occurs frequently in dysfunctional areas of the left ventricle in patients with stable CAD. Hyperenhancement is associated with nonviability by rest-redistribution 201Tl scintigraphy and dobutamine echocardiography, particularly in regions exhibiting resting akinesis/dyskinesis. The absence of hyperenhancement correlates with radionuclide and echocardiographic determinations of viability, regardless of resting contractile function.

Adult↗

PubMed1998

[Biphasic course of left ventricular dysfunction in a 22-year-old female with acute myocarditis].

HISTORY AND CLINICAL FINDINGS: Two days before admission a 22-year-old woman developed general fatigue, nausea, headache and retrosternal pain. Physical examination was unremarkable. INVESTIGATIONS: Erythrocyte sedimentation rate was increased to 20/48, C-reactive protein to 3.3 mg/dl, and there was evidence of myocardial damage (creatine kinase 609 U/l, creatine kinase-MB 42 U/l, troponine T 8.39 ng/ml); ST-segment elevations in I, II, III, aVF and V-V6 of the ECG. Echocardiography revealed clearly thickened myocardium, moderate but haemodynamically not significant pericardial effusion, as well as impaired left ventricular function. Antimyosin scintigraphy was very abnormal. Cardiac catheterization confirmed the left ventricular dysfunction, rise of left ventricular enddiastolic pressure to 17 mm Hg, and a markedly reduced cardiac output of 2.4 l/min. Myocardial biopsy showed severe myocarditis with marked myocytolysis and considerable lymphocytic infiltrations. Enteroviral RNA was demonstrated in the myocardium by polymerase chain reaction. TREATMENT AND COURSE: The haemodynamics became normal within only 3 days. Myocardial biopsy after 6 months was unremarkable histologically and immunohistologically, and left ventricular function was also normal. However, while after a further 12 months myocardial biopsy remained normal and no virus was demonstrated, there was definite, though moderate, impairment in left ventricular function, indicating a dilated cardiomyopathy. INTERPRETATION: Even when histological and immunohistological evidence of healing of an acute viral myocarditis has been achieved, with complete normalization of left ventricular function, a dilated cardiomyopathy may subsequently develop. The pathophysiological mechanism of this occurrence remains unknown.

Acute Disease↗

PubMed1998

Reversible left ventricular dysfunction: does it affect clinical practice and does it matter?

There is substantial evidence that many patients with impaired left ventricular function secondary to coronary artery disease may have hibernating or stunned myocardium. The identification of these patients is important, as revascularisation is associated with an improvement in function, and there is some evidence that revascularisation of these patients will actually improve prognosis. The most useful investigations for the identification of reversible left ventricular dysfunction are dobutamine echocardiography, thallium scanning and, although not available in many centres, PET scanning.

Coronary Disease↗

PubMed2001

Effect of carvedilol on survival and hemodynamics in patients with atrial fibrillation and left ventricular dysfunction: retrospective analysis of the US Carvedilol Heart Failure Trials Program.

BACKGROUND: Atrial fibrillation (AF) is present in a significant number of patients with congestive heart failure (CHF) caused by left ventricular dysfunction and is associated with significant morbidity and increased mortality rates. Thus it is necessary to establish therapy to improve the outcome in this high-risk population. METHODS: We conducted a retrospective analysis of data from the US Carvedilol Heart Failure Trials Program and identified patients with AF at the time of enrollment. In these trials, 1094 patients with at least 3 months of heart failure symptoms and an ejection fraction < or = 0.35 were randomly assigned to receive carvedilol or placebo in a double-blind, stratified program according to performance on an exercise test. RESULTS: One hundred thirty-six patients with concomitant AF and CHF were identified during the screening visit (84 assigned to carvedilol and 52 to placebo). Therapy with carvedilol resulted in a significant improvement in left ventricular ejection fraction (from 23% to 33% with carvedilol and from 24% to 27% with placebo, P =.001). The physician global assessment improved in a greater number of patients treated with carvedilol than in those treated with placebo (71% vs 48%, P =.025). A trend toward a reduction in the combined end point of death or CHF hospitalization was also observed (19% in patients treated with placebo and 7% in patients on carvedilol; relative risk, 0.35; 95% confidence interval, 0.12, 1.02; P =.055). CONCLUSIONS: In patients with AF complicating CHF, carvedilol significantly improves left ventricular ejection fraction and physician global assessment and probably reduces the combined end point of CHF hospitalizations or death.

Adrenergic alpha-Antagonists↗

PubMed1998

Effects of therapy with nifedipine GITS or atenolol on mental stress-induced ischemic left ventricular dysfunction.

OBJECTIVES: We sought to determine the effect of nifedipine gastrointestinal therapeutic system (GITS) or atenolol on ischemic left ventricular dysfunction induced by mental stress. BACKGROUND: The efficacy of conventional antianginal therapy in preventing myocardial ischemia induced by mental stress is unknown. METHODS: Nifedipine GITS, atenolol and placebo were administered to 15 subjects with stable angina in a double-blind crossover trial. Subjects underwent a series of mental stressors at the end of each treatment. Radionuclide ventriculography was performed at baseline and at peak mental stress. Other measured variables included time to ischemia on exercise treadmill testing, ischemia on 48-h ambulatory electrocardiogram (ECG) monitoring, and resting and mental stress-induced levels of plasma catecholamines, tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and platelet aggregability. RESULTS: Mental stress resulted in a significant increase in plasma epinephrine and norepinephrine levels during each treatment phase. Atenolol therapy was associated with lower baseline and postmental stress rate-pressure product compared with nifedipine or placebo. Therapy with either nifedipine GITS or atenolol prevented the development of wall-motion abnormalities and the decline in regional ejection fraction (EF) in the segment with the largest deterioration in wall motion during placebo therapy. Both medications prevented the decrease in global EF in subjects who demonstrated at least a 5% fall in global EF on placebo therapy. No therapy exerted a statistically significant benefit on exercise performance or frequency of ischemia during ambulatory ECG monitoring. CONCLUSIONS: Both nifedipine GITS and atenolol are effective at preventing mental stress-induced wall-motion abnormalities, although the mechanisms may be different.

Adrenergic beta-Antagonists↗

PubMed1988

Beta-blocker therapy in patients with ventricular tachyarrhythmias in the setting of left ventricular dysfunction.

Although several studies suggest beta blockers (BB) are effective in suppressing ventricular arrhythmias, less is known about their role in the treatment of patients with ventricular tachyarrhythmias associated with impaired left ventricular function. To assess the tolerance and efficacy of these agents, 32 patients presenting with either ventricular fibrillation (18) or sustained ventricular tachycardia (14) were studied during BB therapy. Left ventricular dysfunction (mean ejection fraction 29%) was present as a consequence of coronary artery disease (26) or cardiomyopathy (6). Baseline arrhythmia assessment revealed recurrent ventricular tachycardia in all patients. Antiarrhythmic drug therapy including BB was guided by programmed stimulation (10), exercise testing (8), ambulatory monitoring (12), or was given empirically (2). Beta blockers were well tolerated, as measured by exercise duration, which improved significantly, and by long-term maintenance, which continued in 23 of 32 (72%) patients. Over a mean follow-up of 668 days, patients treated with BB had a relatively low incidence of both sudden (3%) and nonsudden (9%) death. Thus, BB can be effective and well tolerated adjunct therapy in patients with a history of ventricular tachyarrhythmias in the setting of impaired left ventricular function.

Adrenergic beta-Antagonists↗

PubMed2003

Plasma atrial natriuretic peptide and brain natriuretic peptide are increased in septic shock: impact of interleukin-6 and sepsis-associated left ventricular dysfunction.

OBJECTIVE: Interest has recently focused on the use of neurohormonal markers such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) as indices of left ventricular systolic dysfunction and prognosis in heart failure. Also, peptides belonging to the interleukin-6 (IL-6) family have been shown to induce ANP and BNP secretion. We hypothesized that BNP and ANP spillover in the peripheral circulation reflects left ventricular dysfunction and IL-6 production in septic shock. DESIGN AND SETTING: Retrospective, clinical study in the medical intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: 17 patients with septic shock and 19 control subjects. INTERVENTIONS: Collection of clinical and demographic data in relation to ANP, BNP, IL-6, and soluble TNF receptors (sTNF-R-p55, sTNF-R-p75) in plasma over a period of 4 days. MEASUREMENTS AND RESULTS: In septic shock we found a significant increase in ANP (82.7+/-9.9 vs. 14.9+/-1.2 pg/ml) and BNP (12.4+/-3.6 vs. 5.5+/-0.7 pg/ml). Plasma ANP peaked together with IL-6. Peaks of ANP and IL-6 were significantly correlated (r=0.73; p<0.01). BNP was inversely correlated to cardiac index (r=-0.56; p<0.05). CONCLUSIONS: ANP and BNP increase significantly in patients with septic shock. BNP reflects left ventricular dysfunction. ANP is related to IL-6 production rather than to cardiovascular dysfunction.

Atrial Natriuretic Factor↗

PubMed1991

Cardiovascular profile of 5 novel nitrate-esters: a comparative study with nitroglycerin in pigs with and without left ventricular dysfunction.

1. Four cumulative 10 min intravenous infusions of 0.05, 0.2, 0.5 and 2.0 mg min-1 were used to compare the cardiovascular profile of 5 novel nitrate-esters dissolved in Intralipid 10% to that of nitroglycerin (GTN) in conscious pigs. 2. Infusion of Intralipid 10% alone had no effect on any of the systemic haemodynamic parameters. GTN infusions decreased mean arterial blood pressure dose-dependently from 94 +/- 2 mmHg to 79 +/- 3 mmHg (P less than 0.05) and raised cardiac output from 2.74 +/- 0.09 l min-1 to 3.40 +/- 0.18 l min-1 (P less than 0.05) due to an increase in heart rate (by up to 43 +/- 3%), as stroke volume decreased slightly. Systemic vascular resistance decreased (by 32 +/- 3%) and left ventricular end-diastolic pressure fell from 5.2 +/- 0.4 mmHg to 2.2 +/- 0.5 mmHg (both P less than 0.05). 3. The novel compounds CEDO 8811, CEDO 8834 and CEDO 8901 increased cardiac output only at the highest dose (7%, 8% and 9%, respectively). There was no change in mean arterial blood pressure as the increase in cardiac output was counterbalanced by arterial vasodilatation. All three compounds reduced left ventricular end-diastolic pressure slightly. 4. CEDO 8816 was a more potent arterial and venodilator than the aforementioned CEDO compounds, as the decreases in systemic vascular resistance and left ventricular end-diastolic pressure were already significant at lower doses. The fall in stroke volume was fully compensated by the increase in heart rate and as a result cardiac output increased by 11 +/- 3% (P less than 0.05) at the highest dose. 5. CEDO 8956 was the most potent vasodilator of the novel compounds and exhibited a cardiovascular profile similar to that of GTN. Left ventricular end-diastolic pressure decreased significantly during infusion of 0.2mgmin-'. Mean arterial blood pressure decreased by 11 +/- 2% (P < 0.05) in spite of an increase in cardiac output by up to 20 +/- 2% (P < 0.05), due to a decrease (by 27 +/- 1%, P <0.05) in systemic vascular resistance. The increases in heart rate (20 +/- 5%, P < 0.05) and LVdP/dtmax (38 +/- 4%, P < 0.05) were, however, considerably less after CEDO 8956 than after GTN. 6. The potential of CEDO 8956 in the treatment of chronic left ventricular dysfunction was evaluated during administration to conscious pigs (21-23 kg), in which the left circumflex coronary artery was ligated 4 weeks earlier. In these animals, baseline values for cardiac output and LVdP/dtx were lower and those of systemic vascular resistance and left ventricular end-diastolic pressure were higher than in the first group of experiments. 7. Both GTN and CEDO 8956 in doses of 0.05 to 2.0 mg inm increased cardiac output dosedependently (by up to 34% and 19%, respectively). The decrease in systemic vascular resistance was larger with GTN (35%) than with CEDO 8956 (17%), which resulted in a 13% decrease in mean arterial pressure during infusion of GTN, whereas there was no change in mean arterial pressure during infusion of CEDO 8956. Both compounds increased LVdP/dt,,,,X (by 48% and 30%, respectively) and lowered left ventricular end-diastolic pressure to normal levels. 8. At a dose of 1.0Omg min- 1, both GTN and CEDO 8956 increased left ventricular blood flow parallel to the increase in myocardial oxygen demand. At this dose, GTN also caused vasodilatation in the vascular beds of the brain, kidneys and adrenals. With CEDO 8956 no significant changes were achieved. 9. We conclude that the cardiovascular profile of CEDO 8956 in both normal animals and in animals with chronic left ventricular dysfunction warrants further study on its usefulness in the treatment of a number of cardiovascular disorders.

Animals↗

PubMed2000

Enoximone echocardiography for predicting recovery of left ventricular dysfunction after revascularization : a novel test for detecting myocardial viability.

BACKGROUND: The possibility that enoximone, a nonglycoside, noncatechol, positive inotropic agent, in combination with 2-dimensional echocardiography may predict recovery of myocardial dysfunction after revascularization has not been yet evaluated. METHODS AND RESULTS: Forty-five patients with chronic coronary artery disease and left ventricular dysfunction underwent dobutamine (DE, 5 to 10 microg. kg(-1). min(-1)) and enoximone (EE, 1.5 mg/kg, over 10 minutes) echocardiography. Myocardial wall motion was scored from 1 (normal) to 4 (dyskinesia): an asynergic segment was considered to have contractile enhancement when the score decreased by >/=1 grade. Of 478 asynergic segments, 216 (45%) exhibited functional recovery after revascularization. Dobutamine- and enoximone-induced contractile enhancement was observed in 41% and 46% of segments, respectively. Compared with DE, EE had higher sensitivity (88% versus 79%, P<0.01) and negative predictive value (90% versus 84%, P<0.05) in predicting functional recovery. The specificity (89% versus 90%) and positive predictive value (87% for both EE and DE) were similar. Concordant interpretation of EE and DE findings was found in 85% (406 of 478) of affected segments. Prerevascularization coronary angiography showed that stenosis severity of vessels supplying areas which only improved with enoximone was significantly greater (89.9%) than that of vessels (77.7%) supplying areas that responded to both agents (P<0.02). Both dobutamine and enoximone increased heart rate (16% and 10%, respectively), whereas enoximone did not cause changes in systolic blood pressure that increased by 14% with dobutamine. CONCLUSIONS: Enoximone echocardiography provides a novel and reliable approach for the prediction of functional recovery after revascularization. Compared with dobutamine echocardiography, the test yields higher sensitivity and induces lesser hemodynamic alterations.

Adult↗

PubMed1994

Right ventricular dysfunction: an independent predictor of adverse outcome in patients with myocarditis.

To assess the predictive value of right ventricular systolic function in patients with active myocarditis, the echocardiograms of 23 patients with biopsy-confirmed myocarditis were reviewed. Right ventricular systolic function was evaluated qualitatively and quantitatively by descent of the right ventricular base. Patients were divided into those with normal right ventricular function, in whom right ventricular descent was 1.9 +/- 0.1 cm, and those with abnormal right ventricular function, in whom right ventricular descent was 0.8 +/- 0.1 cm (p < 0.001). There were no differences between the two groups in age, duration of symptoms, baseline hemodynamics, or histologic assessment. Initial left ventricular ejection fraction was significantly lower in patients with depressed right ventricular function (27.5 +/- 4.9%) compared with that in patients with normal right ventricular function (47.5 +/- 6.3%) (p = 0.01). The likelihood of an adverse outcome, defined as death or need for cardiac transplantation, was greater in patients with abnormal right ventricular function (right ventricular descent < or = 1.7 cm) than in patients with normal right ventricular function (right ventricular descent > 1.7 cm) (p < 0.03). Multivariate analysis revealed that right ventricular dysfunction as quantified by right ventricular descent was the most powerful predictor of adverse outcome.

Female↗

PubMed2004

Brain natriuretic peptide and left ventricular dysfunction in chagasic cardiomyopathy.

Global left ventricular (LV) systolic dysfunction is the strongest predictor of morbidity and mortality in Chagas disease. Echocardiography is considered the gold standard for the detection of LV dysfunction, but not always available in endemic areas where chagasic cardiomyopathy is most common. Brain natriuretic peptide (BNP) is a neurohormone that has been recently described as a simple and inexpensive diagnostic and prognostic marker for patients with congestive heart failure. Chagasic patients (n = 63) and non-infected healthy individuals (n = 18) were recruited prospectively and underwent complete clinical examination, echocardiography and 24-h Holter monitoring. BNP was measured from thawed plasma samples using the Triage BNP test. We observed high levels of BNP in association with depression of LV ejection fraction, with increase of LV end-diastolic diameter and with LV premature complexes. An elevated concentration of BNP, defined as a concentration of 60 pg/ml or more, had a sensitivity of 91.7%, specificity of 82.8%, positive predictive value of 52.4%, and negative predictive value of 98% for detecting LV dysfunction (LV ejection fraction < 40%).BNP measurement using a simple, relatively inexpensive and rapid test has a promising role in identifying LV dysfunction associated with chagasic cardiomyopathy. Equally important, patients with Trypanosoma cruzi infection who have low levels of BNP level in plasma have a very low likelihood of severe cardiac involvement, and echocardiography is probably not necessary.

Adult↗

PubMed2005

Post myocardial infarction, left ventricular dysfunction, and the expanding role of cardiac implantable electrical devices.

In patients post myocardial infarction (MI) at risk for fatal ventricular arrhythmias, cardiac implantable devices offer a means of preventive therapy that complements optimal pharmacologic therapy. In patients with depressed ejection fractions, prophylactic implantable cardioverter defibrillators (ICDs) significantly improve survival. The efficacy of ICDs in the primary prevention of sudden cardiac death in patients post MI has been examined in a number of major primary prevention trials. These trials demonstrated as much benefit as some secondary prevention trials, which were conducted in high-risk patients who already had a spontaneous sustained ventricular tachyarrhythmia. In patients who are candidates for an ICD, best medical therapy for left ventricular dysfunction should be in place for some time before implanting. This waiting period could mean avoiding the implantation of a device in a patient who would heal sufficiently with pharmacologic therapy alone. In New York Heart Association (NYHA) class III and IV, patients with heart failure, and QRS intervals > or = 120 ms, cardiac resynchronization therapy (CRT) in combination with a defibrillator is a valuable addition to optimal pharmacologic therapy. Recent studies have demonstrated improved survival with CRT as well as improved quality of life. The high cost of cardiac implantable devices has led the Centers for Medicare and Medicaid Services to impose strict indications for use. However, it is likely that indications will be broadened for ICDs to include selected patients with left ventricular ejection fraction up to 40%, compared with the current indication of < or = 30%. Implanted devices must be followed up appropriately, with periodic interrogation and program adjustment to reduce the risk for pacing-induced desynchronization and to optimize hemodynamic benefit.

Arrhythmias, Cardiac↗

PubMed2006

Recurrent tako-tsubo-like left ventricular dysfunction (apical ballooning) in a patient with pheochromocytoma - a case report.

Primarily described in Japan, tako-tsubo-like left ventricular dysfunction is a phenomenon characterized by transient apical ballooning in the absence of significant coronary artery disease. The clinical presentation includes symptoms like chest pain, dyspnea, syncope, electrocardiographic changes and elevated myocardial markers, all compatible with the diagnosis of an acute coronary syndrome. The underlying mechanism is supposed to be a catecholamine excess caused by various triggers. We describe a patient with a recurrent tako-tsubo phenomenon, who at work-up proved to have a pheochromocytoma as the most likely underlying disease.

Diagnosis, Differential↗

PubMedDate not supplied

Right ventricular dysfunction secondary to acute massive pulmonary embolism detected by helical computed tomography pulmonary angiography.

OBJECTIVE: Acute massive pulmonary embolism causes abrupt pulmonary arterial hypertension and right ventricular dysfunction (RVD). Patients with RVD have a worse prognosis than those with normal right ventricular function. Consequently, recognizing the RVD at the time of pulmonary embolism is useful for risk stratification and enables more aggressive therapy. The study compared the accuracy of helical computed tomographic (CT) scans with echocardiography in the detecting of RVD in patients with acute massive pulmonary embolism. MATERIALS AND METHODS: Specifically, this work reviewed the CT pulmonary angiograms of 14 patients who were positive for acute massive pulmonary embolism during a 52-month period. CT scans were reviewed for findings indicating RVD. Scans were considered positive for RVD if the right ventricle was dilated or there was leftward shift of the interventricular septum. Echocardiographic reports serving as the reference standard for the diagnosis of RVD were also reviewed. CT study results were then correlated with echocardiography results. RESULTS: Among 14 patients with massive pulmonary embolism, echocardiography identified 12 patients having RVD, whereas the remaining two patients were negative for RVD. Meanwhile, CT correctly identified 11 of 12 patients as having RVD, and was negative for RVD in the remaining 3 patients. Correlated with echocardiography, CT scan for RVD detection had a sensitivity of 91.6% and a specificity of 100%. CONCLUSIONS: CT can accurately detect RVD in patients with acute massive pulmonary embolism. However, this result requires confirmation using a larger prospective cohort study.

Adult↗