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PubMed1997

Performance assessment model for guideline-recommended pharmacotherapy in the secondary prevention of coronary artery disease and treatment of left ventricular dysfunction.

The Agency for Health Care Policy and Research, the National Heart Lung and Blood Institute of the National Institutes of Health, the American Heart Association, and the American College of Cardiology have all developed guidelines for improving the care of patients with cardiovascular disease. The guidelines include recommendations for intensive lipid-lowering therapy in patients with coronary artery disease (CAD) and angiotensin-converting enzyme (ACE) inhibitors in those patients with symptomatic heart failure and asymptomatic left ventricular dysfunction. Despite clinical trial evidence and consensus that these therapies improve survival in high-risk patients, data suggest that there is wide variation in the delivery of guideline-based care. To investigate whether evidence-based assessment of provider practice patterns can impact the delivery of quality cost-effective care, Merck and Company, in conjunction with leading cardiology group practices, the University of North Carolina at Chapel Hill, and Medical Review of North Carolina developed an ambulatory medical record abstraction study. This quality assurance initiative was conducted at practices beginning in the spring of 1996 and continues. Medical records and administrative claims of patients with ischemic heart disease or heart failure were abstracted by a healthcare consulting organization to maintain patient and physician confidentiality. As of mid-July 1997, 626 group practices had completed the medical record abstraction process, with > 1,136 practices participating at some stage of the project; >6,000 physicians participated in the project and >270,000 patients charts were abstracted. Analysis of these data will provide insight and benchmark patterns of care in the pharmacologic management of heart failure and CAD. This project represents a unique collaboration between a pharmaceutical company, an academic institution, a Peer Review Organization, and practicing physicians, to support evidence-based best medical practices.

Aged↗
PubMed1998

[Anatomopathological bases of latent ventricular dysfunction in insulin-dependent diabetics].

INTRODUCTION AND OBJECTIVES: The natural history of diabetic cardiomyopathy remains unclear, mainly due to concurrent coronary disease or hypertension. Since the presence of confounding factors is less likely in youngsters, they constitute a suitable study model to analyze early stages of diabetic cardiomyopathy. PATIENTS AND METHODS: We screened 33 young normotensive asymptomatic patients with type I diabetes mellitus. Mean age was 28 +/- 8 y (range 18 to 46 y) and there were 14 men. RESULTS: 2-D Echo showed normal left ventricular size and wall motion in all patients but one. Radionuclide basal ejection fraction was 56.5 +/- 6.6% and increased to 63 +/- 7.4% (p < 0.02) on exercise. According to Rozansky criteria, 16 patients had an abnormal response. Abnormal stress sestamibi was detected in 18 patients and only 3 had reversible defects. Coronary angiography was performed in 11 patients with at least one abnormal non-invasive study response. Coronary angiography revealed normal vessels in all patients and left anterior descending blood flow velocity (Doppler) increased 4 fold after papaverine infusion. Left ventricular biopsies showed hypertrophy (either nuclear or cellular) in 11, myocytolysis in 6, interstitial fibrosis in 9 and lipid deposits in 4. Morphometric analysis of cardiac samples comparing the diabetic group and a control group showed that the volume fraction of fibrosis (0.19 +/- 0.06 vs 0.10 +/- 0.06; p < 0.01), fiber area -mu2- (1,062 +/- 547 vs 600 +/- 167; p < 0.02) and fiber diameter -mu- (24.2 +/- 3.3 vs 15.1 +/- 3.4; p < 0.001) were higher in the former; and volume fraction of the myocytes was higher in the latter (0.71 +/- 0.006 vs 0.89 +/- 0.07; p < 0.001). CONCLUSIONS: Left ventricular dysfunction, not related to coronary atherosclerosis or small vessel disease, is frequent in asymptomatic young diabetic patients. Abnormal pathologic findings are common in the type of cell hypertrophy, interstitial fibrosis, myocytolysis and lipid deposits.

Adolescent↗
PubMed1995

Effect of long-term enalapril therapy on neurohormones in patients with left ventricular dysfunction. SOLVD Investigators.

The aim of this study was to compare the long-term effects of treatment with enalapril or placebo on plasma neurohormones in patients with left ventricular (LV) dysfunction. Elevated neurohormonal levels are associated with increased mortality in patients with congestive heart failure. Multiple studies have shown that angiotensin-converting enzyme inhibitors decrease mortality and morbidity in these patients. In Studies of Left Ventricular Dysfunction (SOLVD), enalapril significantly reduced mortality in patients with symptomatic LV dysfunction (treatment trial). In contrast, in patients with asymptomatic LV dysfunction (prevention trial), there was no significant reduction in mortality with enalapril therapy. The effect of enalapril was examined in 333 prevention trial and 129 treatment trial patients. Plasma norepinephrine (NE) and plasma renin activity were measured in these patients at baseline, and at 4 and 12 months of follow-up. In a subset of these patients, atrial natriuretic peptide (ANP) and arginine vasopressin were also measured. Analysis of covariance models were used to determine the effect of enalapril on each neurohormone. Participants in the treatment trial had significantly higher neurohormonal levels when compared with those in the prevention trial or normal control subjects. In the treatment trial, patients taking enalapril had a greater decrease in plasma NE levels than patients taking placebo (p < 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

[The effectiveness of enoximone in patients with serious left ventricular dysfunction submitted for aorto-coronary bypass].

BACKGROUND: The purpose of this study was to investigate whether the combined positive inotropic and vasodilating properties of enoximone have a short-term benefit when used in patients who underwent open heart surgery. METHODS: From 7/1994 to 1/1995 twenty-six patients with severe myocardial dysfunction (ejection fraction < 35%) were enrolled into a prospective trial before undergoing coronary artery bypass graft. They were randomly selected into two study groups: the first treated with enoximone (group E) and the other one with dopamine (group D). Anaesthesia was the same for both groups using high-dose fentanyl. Buckberg cardioplegia was used. All patients were followed by: conventional monitoring, Swan-Ganz catheter and transesophageal echocardiography. measurements (hemodynamic parameters, end-systolic and diastolic area and left ventricular wall motion) were recorded: after induction of anesthesia, after loading-dose and an intensive care unit. Enoximone- and dopamine infusions were started during weaning from cardiopulmonary bypass and tailored to hemodynamic parameters (cardiac index > 2.8 l/min, wedge pressure < 16 mmHg, mixed venous blood saturation > 65%). Major events were defined as: endotracheal intubation > 36 h, using intraortic balloon pump or centrifugal pump, intensive care timer > 48 h, in hospital cardiac death. Prices, were established by DRG-tables (diagnosis related groups). Statistical analysis were performed by X and "t" Student tests. RESULTS: Cardiac index increased more significantly in group E (CI 1.9-->3.9 vs 2.3-->3.3; p 0.05) thanks to a higher reduction of vascular systemic (SVRI 2889-->1447 vs 2536 -->1565; p 0.005) and pulmonary resistances (PVRI 271-->193 vs 288-->218; p 0.05). Fewer major cumulative events and intensive care costs were observed in group E rather than group D. CONCLUSIONS: Enoximone administer immediately after open heart surgery had more beneficial hemodynamic and clinical effects than dopamine in patients with severe left ventricular dysfunction.

Cardiotonic Agents↗
PubMed1997

Premorbid determinants of left ventricular dysfunction in a novel model of gradually induced pressure overload in the adult canine.

BACKGROUND: When a pressure overload is placed on the left ventricle, some patients develop relatively modest hypertrophy whereas others develop extensive hypertrophy. Likewise, the occurrence of contractile dysfunction also is variable. The cause of this heterogeneity is not well understood. METHODS AND RESULTS: We recently developed a model of gradual proximal aortic constriction in the adult canine that mimicked the heterogeneity of the hypertrophic response seen in humans. We hypothesized that differences in outcome were related to differences present before banding. Fifteen animals were studied initially. Ten developed left ventricular dysfunction (dys group). Five dogs maintained normal function (nl group). At baseline, the nl group had a lower mean systolic wall stress (96 +/- 9 kdyne/cm2; dys group, 156 +/- 7 kdyne/cm2; P < .0002) and greater relative left ventricular mass (left ventricular weight [g]/body wt [kg], 5.1 +/- 0.36; dys group, 3.9 +/- 0.26; P < .02). On the basis of differences in mean systolic wall stress at baseline, we predicted outcome in the next 28 dogs by using a cutoff of 115 kdyne/cm2. Eighteen of 20 dogs with baseline mean systolic stress > 115 kdyne/cm2 developed dysfunction whereas 6 of 8 dogs with resting stress < or = 115 kdyne/cm2 maintained normal function. CONCLUSIONS: We conclude that this canine model mimicked the heterogeneous hypertrophic response seen in humans. In the group that eventually developed dysfunction there was less cardiac mass despite 60% higher wall stress at baseline, suggesting a different set point for regulating myocardial growth in the two groups.

Animals↗
PubMed2005

Right ventricular dysfunction in chronic dilated cardiomyopathy and heart failure.

In patients with advanced heart failure, the main focus has traditionally been placed on the functional assessment of the left ventricle. Therefore, the current body of literature examining the right ventricle and its influence on the pathophysiological processes in heart failure has been limited. Methods currently employed to assess the size and function of the right ventricle include: high frequency thermodilution, contrast ventriculography, radionuclide ventriculography, echocardiography, and magnetic resonance imaging; however, none of these techniques has proven to be a 'gold standard' for the assessment of right ventricular function. Nevertheless, when these methods are employed, right ventricular dysfunction has been shown to be a powerful predictor of reduced exercise capacity and survival. This relationship holds true for patients with heart failure secondary to either ischemic or non-ischemic dilated cardiomyopathy.

Cardiomyopathy, Dilated↗
PubMed2003

Trandolapril in left ventricular dysfunction after myocardial infarction: focus on the TRACE study.

The new angiotensin-converting enzyme (ACE) inhibitor trandolapril has been the subject of a broad pharmacological and clinical development program. The active metabolite, trandolaprilat, has been found to have a high level of affinity for angiotensin-converting enzyme. Trandolapril has demonstrated potent ACE inhibition, a long plasma half-life and a high degree of lipophilicity. The drug has been used to treat patients with mild-to-moderate hypertension and congestive heart failure following myocardial infarction. In the former patients, a once-daily dosage of trandolapril has produced significant and long-lasting reductions in blood pressure and has reduced left ventricular hypertrophy. Trandolapril is one of a few ACE inhibitors with a mean trough:peak ratio of blood pressure reduction with once-daily administration of over 50%. In addition, studies in hypertensive patients have revealed still greater reductions in blood pressure when trandolapril is combined with the calcium antagonist verapamil. In patients with left ventricular dysfunction after myocardial infarction, the large TRACE trial showed that mortality was reduced and life expectancy increased with trandolapril treatment.

Animals↗
PubMed2001

Myocardial revascularization in patients with severe ischemic left ventricular dysfunction. Long term follow-up in 141 patients.

OBJECTIVES: The present study evaluates our experience with coronary bypass grafting in patients with EF < or =25%. Myocardial revascularization in this setting remains controversial because of concerns over operative mortality and morbidity and lack of functional and survival benefit. MATERIALS AND METHODS: One hundred and forty-one patients with coronary artery disease and left ventricular ejection fraction < or =25% underwent coronary artery bypass graft between January 1988 and December 1998. Mean age at operation was 63.3 years and 81.4% were male. The major indication for surgery was angina (114 patients, 80.8%). Ejection fraction (EF), left ventricular end diastolic pressure (LVEDP) and cardiac index (CI) were used to assess left ventricular function. The number of graft was 2.7+/-1.6/patient. Internal mammary artery was used in 119 patients (84.3%). Intra aortic balloon pump was placed preoperatively in 25 patients (17.7%). Five operative risk factors were associated with a higher mortality: emergency, female sex, LVEDP, CI and NYHA class IV. RESULTS: The operative mortality was 7% (10 patients). Left ventricular ejection fraction (assessed post operatively in 83 patients) improved from 22.2% preoperatively to 33.5% post operatively (P<0.001), mean end diastolic volume index fell from 98 to 83 ml/m(2) following surgery. Survival at 2, 5 and 7 years was respectively 84+/-3%, 70+/-4% and 50+/-5%. Two variables were associated with increased long term survival: congestive heart failure (NYHA class lower than IV (P=0.035) and cardiomegaly (P=0.04) CONCLUSION: In patients with left ventricular dysfunction, myocardial revascularization can be performed relatively safely with good medium term survival and improvement in quality of life and in left ventricular function. Coronary artery bypass graft may be offered to patients with impaired ventricular function, but careful patient selection and management when considering these patients for operation should assess potentially reversible dysfunction.

Adult↗
PubMed2003

Transforming growth factor beta and diastolic left ventricular dysfunction after heart transplantation: echocardiographic and histologic evidence.

BACKGROUND: The mechanism for chronic left ventricular diastolic dysfunction in the non-rejecting cardiac allograft has not been fully studied. OBJECTIVES: The purposes of this study were to analyze the significance and frequency of left ventricular diastolic dysfunction after heart transplantation and to examine the involvement of fibrotic cytokines (transforming growth factor beta [TGF-beta]) in development of clinical and echocardiographic changes in cardiac allograft recipients. METHODS: We studied 152 heart transplant recipients who had survived for at least 24 months. We compared histopathologic findings (staining of endomyocardial biopsy specimens using hematoxylin and eosin, and polyclonal antibodies expressed as TGF-beta score), left ventricular function (Doppler echocardiography), and clinical course (New York Heart Association [NYHA] status). We classified patients into Group 1 (n = 41 recipients) with a restrictive filling pattern, mitral deceleration time (MDT) <140 milliseconds, and Group 2 (n = 111 recipients), MDT >or=140 milliseconds. RESULTS: The MDT was 122 +/- 7 milliseconds in Group 1 compared with an MDT of 177 +/- 17 milliseconds in Group 2 (p = 0.0003). Group 1 showed significant immunohistochemical staining in endomyocardial biopsy specimens (a mean TGF-beta score of 9.1 +/- 1.2 for Group 1 compared with a mean TGF-beta score of 3.6 +/- 0.8 for Group 2 p = 0.001). The TGF-beta expression correlated inversely with both MDT and isovolumic relaxation time (r = -0.77, p = 0.0004, and r = -0.69, p = 0.004, respectively). Mean NYHA status in Group 1 recipients was 2.2 +/- 1.1 compared with 1.37 +/- 0.6 for Group 2 (p = 0.006). CONCLUSIONS: Transforming growth factor beta expression in cardiac allografts is associated with impaired left ventricular diastolic function. The pathogenesis of diastolic dysfunction may be an aberrant repair process after rejection-caused TGF-beta expression in the allograft.

Adult↗
PubMed2005

Left ventricular dysfunction after acute intracranial hypertension is associated with increased hydroxyl free radical production, cardiac ryanodine hyperphosphorylation, and troponin I degradation.

BACKGROUND: In addition to generating free radicals, stress-induced activation of the sympathetic nervous system results in hyperphosphorylation of the cardiac ryanodine receptor (RyR2)/calcium (Ca2+) release channel on the sarcoplasmic reticulum, causing leaky channels. These events may contribute to cytosolic Ca2+ overload and activation of Ca2+-dependent cytotoxic processes. Because myocardial dysfunction associated with intracranial hypertension is catecholamine mediated, we sought to determine in a rat model if hemodynamic changes are associated with an increase in oxidative stress, hyperphosphorylation of RyR2, and degradation of myofilament protein cardiac troponin I (TnI). METHODS: In halothane-anesthetized rats treated with saline, dimethyl sulfoxide (DMSO), or the synthetic calpain inhibitor calpeptin (3,500 microg), a subdural balloon catheter was inflated to induce intracranial hypertension. Hearts were excised, and RyR2 phosphorylation status and TnI degradation was determined with Western blot analysis. In separate experiments, treated rats were challenged with increasing doses of dobutamine 30 minutes after subdural balloon inflation. RESULTS: Elevating the intracranial pressure resulted in an increase in plasma catecholamines, as well as in 3,4-dihydroxybenzoic acid (DHBA), an indirect marker of HO. radical production, and left ventricular dysfunction in rats treated with saline or DMSO. There was evidence of hyperphosphorylation of RyR2 and TnI degradation (27 kD immunoreactive band). Calpeptin treatment improved left ventricular function; however, this had no effect on the phosphorylation status of RyR2 or TnI degradation levels. In addition, the myocardial responsiveness to dobutamine was augmented in rats with depressed myocardial function. CONCLUSION: The present findings demonstrate that hemodynamic instability after intracranial hypertension is associated with oxidative stress and post-translational changes to RyR2 and TnI degradation. Despite this, the myocardial responsiveness to beta1 adrenergic stimulation is preserved in rats with depressed myocardial function.

Acute Disease↗
PubMed1999

Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction.

BACKGROUND: Impaired alveolar-capillary membrane conductance is the major cause for the reduction in pulmonary diffusing capacity for carbon monoxide (DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmonary microvascular damage, or is variable is unknown. The aim of this study was to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects of volume loading on airflow rates. METHODS AND RESULTS: Ten patients with left ventricular dysfunction (LVD) and 8 healthy volunteers were studied. DM and Vc were determined by the Roughton and Forster method. The forced expiratory volume in 1 second (FEV1), vital capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL. kg-1 body wt of 0.9% saline acutely reduced DM (12.0+/-3.3 versus 10.4+/-3.5 mmol. min-1. kPa-1, P<0.005), FEV1 (2.3+/-0.4 versus 2.1+/-0.4 L, P<0.0005), and PEFR (446+/-55 versus 414+/-56 L. min-1, P<0.005). All pulmonary function tests had returned to baseline values 24 hours later. In normal subjects, saline infusion had no measurable effect on lung function. CONCLUSIONS: Acute intravascular volume expansion impairs alveolar-capillary membrane function and increases airflow obstruction in patients with LVD but not in normal subjects. Thus, the abnormalities of pulmonary diffusion in heart failure, which were believed to be fixed, also have a variable component that could be amenable to therapeutic intervention.

Aged↗
PubMed1999

Regional left ventricular dysfunction in a patient with severe prolonged anemia.

A 47-year-old woman with severe prolonged anemia developed heart failure. After treatment of the heart failure and anemia, she showed regional dysfunction of the left ventricular wall and myocardial fatty acid metabolism was disturbed in these sites. Coronary arteriography showed normal images. It took about 4 months to recover both left ventricular wall motion and fatty acid metabolism. Prolonged decrease of oxygen supply to the myocardium, which is caused by severe prolonged anemia, seemed to affect the myocardial function in this case, which could be another model of anemia-related myocardial dysfunction.

Anemia↗
PubMed2005

Phosphodiesterase-5 inhibition with sildenafil attenuates cardiomyocyte apoptosis and left ventricular dysfunction in a chronic model of doxorubicin cardiotoxicity.

BACKGROUND: Sildenafil, a phosphodiesterase-5 inhibitor, induces cardioprotection against ischemia/reperfusion injury via opening of mitochondrial K(ATP) channels. It is unclear whether sildenafil would provide similar protection from doxorubicin-induced cardiotoxicity. METHODS AND RESULTS: Male ICR mice were randomized to 1 of 4 treatments: saline, sildenafil, doxorubicin (5 mg/kg IP), and sildenafil (0.7 mg/kg IP) plus doxorubicin (n=6 per group). Apoptosis was assessed with the use of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and in situ oligo ligation methods. Desmin distribution was determined via immunofluorescence. Bcl-2 expression was analyzed by Western blot. Left ventricular function was assessed by measuring developed pressure and rate pressure product in Langendorff mode. ECG changes indicative of doxorubicin cardiotoxicity were also measured. For in vitro studies, adult ventricular cardiomyocytes were exposed to doxorubicin (1 micromol/L), sildenafil (1 micromol/L) with or without N(G)-nitro-L-arginine methyl ester (L-NAME) (100 micromol/L), or 5-hydroxydecanoate (100 micromol/L) 1 hour before doxorubicin and incubated for 18 hours. Doxorubicin-treated mice demonstrated increased apoptosis and desmin disruption, which was attenuated in the sildenafil+doxorubicin group. Bcl-2 was decreased in the doxorubicin group but was maintained at basal levels in the sildenafil+doxorubicin group. Left ventricular developed pressure and rate pressure product were significantly depressed in the doxorubicin group but were attenuated in the sildenafil+doxorubicin group. ST interval was significantly increased in the doxorubicin group over 8 weeks. In the sildenafil+doxorubicin group, ST interval remained unchanged from baseline. Doxorubicin caused a significant increase in apoptosis, caspase-3 activation, and disruption of mitochondrial membrane potential in vitro. In contrast, sildenafil significantly protected against doxorubicin cardiotoxicity; however, this protection was abolished by both L-NAME and 5-hydroxydecanoate. CONCLUSIONS: Prophylactic treatment with sildenafil prevented apoptosis and left ventricular dysfunction in a chronic model of doxorubicin-induced cardiomyopathy.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2005

Chylous ascites as the main manifestation of left ventricular dysfunction: a case report.

BACKGROUND: Ascites is one of the most common complications of liver diseases, even though in 15% of the cases it is related to extrahepatic diseases; 3% are of cardiac nature and they appear associated with signs and symptoms of heart failure. CASE PRESENTATION: A 70 year old man was admitted with more than one year history of abdominal distension and a weight gain of 10 kilograms. He is asymptomatic and walks 2000-3000 meters a day without angor or dyspnea. The physical examination shows moderate abdominal distension, with no hepatosplenomegaly or edema, and there is mild jugular vein distension. The studies performed (complete laboratory work up, paracentesis, liver biopsy, echocardiogram, intrahepatic pressure measurements, etc.) showed a chylous ascites related to portal hypertension, and left ventricular dysfunction was the only probable cause found. CONCLUSION: Asymptomatic heart dysfunction can mimic liver disease and should be kept in mind as a cause of chylous ascites.

Aged↗
PubMed2004

Ischemic and viable myocardium in patients with non-Q-wave or Q-wave myocardial infarction and left ventricular dysfunction: a clinical study using positron emission tomography, echocardiography, and electrocardiography.

OBJECTIVES: We investigated whether patients with non-Q-wave myocardial infarction (NQMI) have more ischemic viable myocardium (IVM) than patients with Q-wave myocardial infarction (QMI). BACKGROUND: Non-Q-wave myocardial infarction is associated with higher incidences of cardiac events than QMI, suggesting more myocardium at risk in NQMI. METHODS: To identify myocardial ischemia, hibernation, and scar, the resting and stress (82)rubidium perfusion and F-18 fluorodeoxyglucose metabolic positron emission tomographic imaging (PET) was performed in 64 consecutive patients with NQMI (n = 21) or QMI (n = 43). Echocardiography was performed for assessment of left ventricular function and wall motion index (WMI). The relationships between PET, echocardiographic, and electrocardiographic findings were analyzed. RESULTS: There were no significant differences in left ventricular ejection fraction (LVEF) between NQMI and QMI groups (28 +/- 10% vs. 25 +/- 11%, p > 0.05). Ischemic and viable myocardium was more common in NQMI than in QMI (91% vs. 61%, p < 0.05). The total amount of IVM was significantly higher in NQMI than in QMI (6.5 +/- 5.2 vs. 2.9 +/- 2.8 segments, p < 0.001). Neither the number of Q waves, residual ST-segment depression of >or=0.5 mm or elevation of >or=1 mm, nor LVEF and WMI were significant predictors for IVM. Wall motion index correlated with scar segments (r = 0.54, p < 0.001) and LVEF (r = -0.67, p < 0.001). CONCLUSIONS: Ischemic and viable myocardium is common in patients with NQMI and left ventricular dysfunction, suggesting that aggressive approaches should be taken to salvage the myocardium at risk in such patients.

Case-Control Studies↗
PubMed2005

Usefulness of latent left ventricular dysfunction assessed by Bowditch Treppe to predict stress-induced pulmonary hypertension in minimally symptomatic severe mitral regurgitation secondary to mitral valve prolapse.

We assessed whether the presence of latent myocardial dysfunction, evaluated by echocardiographic derived force-frequency relationship (FFR) during exercise, predicts the appearance of stress-induced pulmonary hypertension in minimally symptomatic patients with severe mitral regurgitation (MR). Two groups of patients were identified: group I with normal (</=40 mm Hg) and group II with abnormal (>40 mm Hg) peak stress systemic pulmonary artery pressure. Group I had normal and upsloping FFR and group II had abnormal flat or biphasic FFR. Therefore, in patients with severe MR and apparently normal left ventricular function, the stress-induced pulmonary hypertension seems to be related to the presence of latent left ventricular dysfunction.

Analysis of Variance↗
PubMed2002

Reversible left ventricular dysfunction "takotsubo" cardiomyopathy related to catecholamine cardiotoxicity.

An 80-year-old female was admitted for a persistent consciousness disturbance. Electrocardiography revealed ST-segment elevation in leads II, III, aVf, and V3-V6. Coronary angiography demonstrated normal arteries, while left ventriculography revealed asynergy of apical akinesis and basal hyperkinesis. The creatinine kinase and creatinine kinase MB levels were not elevated after the initial measurement on admission. The diffuse ST-segment elevation reached a maximum level 24 hours after admission. In leads V3-V6, ST-segment elevation continued for 48 hours, and was followed-up by deep inverted T waves. Within 24 days, the asynergy improved without any specific treatment, but the giant negative T waves were present on the electrocardiogram. The plasma norepinephrine and brain natriuretic peptide levels on the first hospital day were 2.9ng/mL and 906pg/mL, respectively. The left ventricular dysfunction appeared to be induced by the exposure to high-level plasma catecholamines. (123)I-metaiodobenzyl guanidine scintigraphy also revealed transient dysfunction of the cardiac catecholamine dynamics.

Aged↗
PubMed2004

[Diabetes mellitus, left ventricular dysfunction and congestive heart failure].

Diabetes is a well known risk factor for the development of congestive heart failure. Epidemiological evidence in the community underscores the prevalence of left ventricular systolic dysfunction in diabetic patients as 2-fold with respect to non-diabetic ones, with half of them completely asymptomatic. Diastolic dysfunction in diabetic hearts, in comparison with non-diabetic, is even more frequent. The high prevalence has been explained by the frequent coexistence of an underlying diabetic cardiomyopathy, hypertension and ischemic heart disease. In these patients, the diabetic metabolic derangement, together with the early activation of sympathetic nervous system, induce a decrease of myocardial function. The activation of renin-angiotensin system results in an unfavorable cardiac remodeling. The progression from myocardial damage to overt dysfunction and heart failure is often asymptomatic for a long time and frequently undiagnosed and untreated. Currently, the widespread availability of echocardiography and possibly the use of cardiac natriuretic peptides, may allow for an earlier recognition of most of such patients. In heart failure, diabetic patients have a worse prognosis than non-diabetics. The available pharmacological treatments, such as ACE-inhibitors, beta-blockers and possibly angiotensin receptor blockers, togheter with a tight glycemic control, may be effective to reverse the remodeling process and prevent cardiovascular events. In order to identify most of the diabetic patients at risk of development of left ventricular dysfunction and to prevent its progression to overt heart failure, it seems important to elaborate a screening strategy in order to diagnose and treat most of diabetic patients with myocardial damage.

Diabetes Complications↗