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PubMed2000

Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. ACE-Inhibitor Myocardial Infarction Collaborative Group.

BACKGROUND: We undertook a prospective systematic overview based on data from individual patients from five long-term randomised trials that assessed inhibitors of angiotensin-converting enzyme (ACE) in patients with left-ventricular dysfunction or heart failure. METHODS: Three of the trials enrolled patients within a week after acute myocardial infarction. Data were combined by use of the Peto-Yusuf method. FINDINGS: Overall 12,763 patients were randomly assigned treatment or placebo and followed up for an average of 35 months. In the three post-infarction trials (n=5,966), mortality was lower with ACE inhibitors than with placebo (702/2995 [23.4%] vs 866/2971 [29.1%]; odds ratio 0.74 [95% CI 0.66-0-83]), as were the rates of readmission for heart failure (355 [11.9%] vs 460 [15.5%]; 0.73 [0.63-0.85]), reinfarction (324 [10.8%] vs 391 [13.2%]; 0.80 [0.69-0.94]), or the composite of these events (1049 [35.0%] vs 1244 [41.9%]; 0.75 [0.67-0.83]; all p<O.001). For all five trials the ACE inhibitor group had lower rates of death than the placebo group (1,467/6,391 [23.0%] vs 1,710/6,372 [26.8%]; 0.80 [0.74-0.87]) and lower rates of reinfarction (571 [8.9%] vs 703 [11.0%]; 0.79 [0.70-0.89]), readmission for heart failure (876 [13.7%] vs 1202 [18.9%]; 0.67 [0.61-0.74]), and the composite of these events (2161 [33.8%] vs 2610 [41.0%]; 0.72 [0.67-0.78]; all p<0.0001). The benefits were observed early after the start of therapy and persisted long term. The benefits of treatment on all outcomes were independent of age, sex, and baseline use of diuretics, aspirin, and beta-blockers. Although there was a trend towards greater reduction in risk of death or readmission for heart failure in patients with lower ejection fractions, benefit was apparent over the range examined.

Aged↗
PubMed1992

[The relationship between anomalies in the autonomous nervous system and left ventricular dysfunction in patients with hypertrophic cardiomyopathy].

This study was undertaken to assess autonomic nervous system (ANS) activity and its relation to left ventricular function in 40 patients (mean age: 41 +/- 17 years) with hypertrophic cardiomyopathy (HC), in sinus rhythm, off-drugs. Patients were grouped according to the results of radionuclide angiography: 26 had an ejection fraction > 50% (Group A), whereas 14 had an ejection fraction < or = 50% (Group B). Evaluation of parasympathetic activity showed abnormalities in: heart rate (HR) response during Valsalva (< or = 1.1) in 2 Group A (8%) and 12 Group B (86%) patients (p < 0.001); HR variability during deep breathing (< or = 10 b/min) in 2 Group A (8%) and 14 Group B (100%) patients (p < 0.001); immediate HR response to standing (30:15 < or = 1.0) in 2 Group A (8%) and 6 Group B (43%) patients (p < 0.025). Assessment of sympathetic activity showed abnormalities in: systolic blood pressure fall to standing (> 20 mmHg) in 2 Group B (14%) patients only (NS); diastolic blood pressure response to handgrip (< 10 mmHg) in 4 Group B (29%) patients only (p < 0.025). Thus, in HC: impaired parasympathetic control is common in those patients showing left ventricular dysfunction; concurrent sympathetic abnormality may also occur in this subgroup of patients; ANS dysfunction seems to be merely an epiphenomenon which marks the severity of left ventricular derangement.

Adult↗
PubMed1997

Inhibition of carnitine synthesis protects against left ventricular dysfunction in rats with myocardial ischemia.

During myocardial ischemia, inhibition of the carnitine-mediated transportation of fatty acid may be beneficial because it facilitates glucose utilization and prevents an accumulation of fatty acid metabolites. We orally administered 3-(2,2,2-trimethyl hydrazinium) propionate (MET), an inhibitor of carnitine synthesis, for 20 days to rats. Then we evaluated left ventricular (LV) function during brief ischemia by using a buffer-perfused isovolumic heart model. After 15 min of reoxygenation after the transient ischemia, LV peak systolic pressure (PSP) almost completely returned to the baseline level in rats given MET (96 +/- 4%), whereas it was only partially (77 +/- 16%) recovered in the placebo-treated rats. We induced myocardial infarction in other rats by ligating the left anterior descending coronary artery. Then the animals were given MET for 20 days, and LV function was compared. In the placebo-treated rats (with myocardial infarction, but without drug treatment), LVPSP was lower than that in the sham group [108 +/- 19 (n = 10) vs. 136 +/- 15 mm Hg (n = 13); p < 0.05], and the time constant (T) of LV pressure decay was elongated (36 +/- 4 vs. 30 +/- 7 ms; p < 0.05). In MET-treated groups, however, neither PSP nor T differed from those in the sham group. In conclusion, inhibition of the carnitine-mediated transportation of fatty acid by MET protected against left ventricular dysfunction in acute and chronic myocardial ischemia.

Animals↗
PubMed1996

[Tolerance of amlodipine in left ventricular dysfunction of ischemic origin].

The aim of this study was to assess the effects of amlodipine on left ventricular function at rest and on effort, at least 30 days after myocardial infarction. The 30 patients included in the study had resting isotopic ejection fractions of 40 to 60%. At inclusion and after 15 days treatment with 10 mg of amlodipine, the patients underwent exercise stress testing with a standard Bruce protocol and resting and exercise isotopic left ventricular ejection fractions were measured. The association of betablockers was allowed but vasodilator therapy was prohibited. During the second exercise stress test, the duration of exercise increased (437 +/- 167 to 518 +/- 154 s; p < 0.002) and the work level rose from 140 +/- 56 to 169 +/- 60 Watts; p < 0.04. The number of electrically positive tests did not change significantly (33 vs 26.7%; NS). The resting ejection fraction did not increase after 15 days treatment with amlodipine (47.4 +/- 6.7 vs 48.3 +/- 8.9%; NS). Similar results were observed with respect to the exercise ejection fraction (51.4 +/- 10.4 vs 52.6 +/- 8.6%; NS). These patients may however be divided into two subgroups. In the first subgroup of 10 patients, the resting ejection fraction rose by more than 5% with amlodipine whereas the exercise ejection fraction remained unchanged (54.4 +/- 7.7% vs 54.5 +/- 7.5% with amlodipine). In the second subgroup of 20 patients, the resting ejection fraction decreased slightly with amlodipine (48 +/- 6.9% vs 45.3 +/- 8%; p = 0.04) but increased significantly on exercise (45.3 +/- 8% vs 51.7 +/- 9.1%; p < 0.0002). Therefore, amlodipine, a new generation calcium antagonist, does not induce any deleterious effect after myocardial infarction with mild left ventricular dysfunction.

Adult↗
PubMed2005

Implantable cardioverter-defibrillator efficacy in patients with heart failure and left ventricular dysfunction (from the MADIT II population).

The Multicenter Automatic Defibrillator Implantation Trial II demonstrated a significant 31% reduction in the risk of mortality in postinfarction patients with low ejection fraction (EF < or =30%). Recently, results from the Sudden Death in Heart Failure Trial indicated that a subgroup of patients with New York Heart Association (NYHA) class III heart failure had less benefit from an implantable cardioverter-defibrillator (ICD) than patients with less advanced heart failure. This study evaluates the association between NYHA class, EF, and blood urea nitrogen (BUN) levels as measures of heart failure and left ventricular dysfunction, and ICD benefit in reducing mortality as well as the association of these parameters with ICD therapy for ventricular tachyarrhythmias. NYHA class I was identified in 442 patients (36%), class II in 425 (35%), and class III in 350 patients (29%). EF < or =20% was present in 472 patients (38%), EF of 21% to 25% in 359 patients (29%), and EF of 26% to 30% in 401 patients (33%). BUN < or =25 mg/dl was present in 850 patients (70%) and >25 mg/dl in 368 patients (30%). Patients with higher NYHA class and BUN had higher mortality (34%) and a higher risk of arrhythmic events (33% to 35%) than patients in lower functional groups (16% to 20%). EF did not differentiate the risk. There was no evidence for significant interactions between mortality, ICD therapy, and tested parameters. In conclusion, patients with more advanced heart failure have a higher risk of mortality and arrhythmic events than patients with less severe disease. However, there is no significant difference in the benefit from ICD therapy among the above subgroups of patients in the Multicenter Automatic Defibrillator Implantation Trial.

Aged↗
PubMed2002

Reversible left ventricular dysfunction "takotsubo" cardiomyopathy associated with pneumothorax.

An 83 year old woman presented to the emergency department with chest pain and dyspnoea. Chest radiography showed pneumothorax of the left lung. Arteries were normal on coronary angiography. Left ventriculography showed asynergy of apical akinesis and basal hyperkinesis. Within 18 days, the asynergy improved without any specific treatment. In the present case the left ventricular dysfunction may have been induced by altered catecholamine dynamics as a result of pneumothorax.

3-Iodobenzylguanidine↗
PubMed1996

Myocardial defect detected by 123I-BMIPP scintigraphy and left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy.

The present study examined the role of myocardial fatty acid in patients with idiopathic cardiomyopathy (DCM) by means of 123I-beta-methyl-p-iodophenyl pentadecanoic acid (123I-BMIPP) scintigraphy. Thirteen patients underwent 123I-BMIPP imaging, 201Tl imaging and echocardiography. All patients showed defective myocardial uptake of 123I-BMIPP and 201Tl. The left ventricular end-diastolic dimension (64.1 +/- 7.3 mm vs. 55.6 +/- 1.5 mm, p < 0.05) and end-systolic dimension (52.4 +/- 8.0 mm vs. 40.6 +/- 2.1 mm, p < 0.01) were significantly large in the defect group (123I-BMIPP defect score (DS) > 8) than the small defect group (DS < 7). The % fractional shortening (%FS) was also significantly smaller (18.6 +/- 3.8% vs. 27.0 +/- 3.3%, p < 0.01) in the large defect group. The 123I-BMIPP DS correlated statistically with %FS (r = 0.75, p < 0.01), while the 201Tl DS did not (r = 0.41, ns). We conclude that the patients with DCM revealed a 123I-BMIPP uptake defect and the defect reflected the degree of left ventricular dysfunction.

Adult↗
PubMedDate not supplied

Is abnormal iodine-123-MIBG kinetics associated with left ventricular dysfunction in patients with diabetes mellitus?

BACKGROUND: Although autonomic neuropathy is frequently recognized in patients with diabetes mellitus, it is uncertain whether cardiac sympathetic neuropathy may play a role in the development of diabetic cardiomyopathy. METHODS AND RESULTS: In 10 control subjects and 61 patients with diabetes mellitus who did not have coronary artery disease, cardiac sympathetic function and left ventricular ejection fraction (LVEF) were evaluated by using iodine-123-metaiodobenzylguanidine (MIBG) imaging and echocardiography, respectively. Dynamic acquisitions and planar images obtained 15 and 150 minutes after injection were used as a means of measuring early and late myocardial uptake and clearance rates of MIBG from the heart. Eight patients with an LVEF less than 50% demonstrated a lower late myocardial MIBG uptake (0.0043% +/- 0.0017% vs. 0.0024% +/- 0.0009%/pixel, P = .002) and a higher clearance rate (22.9% +/- 17.7% vs. 49.3% +/- 12.2%, P<.0001) than the 53 patients with an LVEF of 50% or greater, although the age, sex, type of diabetes mellitus, and frequency of neuropathy, retinopathy, and nephropathy were not significantly different between the 2 subgroups. The LVEF correlated weakly but significantly with early and late myocardial uptake and clearance rate (r = 0.277, P = .03; r = 0.421, P = .001; r = 0.382, P = .002; respectively) in patients with diabetes mellitus. CONCLUSION: Marked MIBG abnormalities are associated with left ventricular dysfunction in patients with diabetes mellitus. However, long-term follow-up of patients with diabetes mellitus who have marked MIBG abnormalities and normal LVEF will be required to determine whether these patients would demonstrate systolic dysfunction earlier than patients without an MIBG abnormality.

3-Iodobenzylguanidine↗
PubMed1999

Left ventricular dysfunction during dobutamine stress echocardiography in patients with syndrome X and positive myocardial perfusion scintigraphy.

AIMS: A sizeable proportion of patients with angina, angiographically smooth coronary arteries and positive exercise test (syndrome X) have stress/rest myocardial perfusion defects. The aim of the study was to assess whether perfusion defects are dependent upon a reduction in coronary flow reserve causing regional left ventricular dysfunction in syndrome X patients. METHODS AND RESULTS: Twenty-two syndrome X patients underwent dobutamine stress echocardiography (DSE). All had stress-induced perfusion defects documented by 99m-Tc-MIBI scintigraphy. Resting and peak DSE wall motion score index (WMSI) were evaluated. Six patients exhibited resting wall motion abnormalities in 10 segments (WMSI 1.05 +/- 0.11). DSE was positive in 12 patients (53%), in whom 16 myocardial segments were involved: of these, 12 were normokinetic and 4 hypokinetic at rest. Peak WMSI was 1.17 +/- 0.17 (p < 0.05 vs rest). Of the 12 patients with a positive DSE, 9 also showed diagnostic ECG changes and 6 complained of angina. Of the 10 patients with negative DSE, 5 had angina and 5 (one with angina) showed ECG changes. In 7 patients (7 segments) (32%), the location of dobutamine-induced wall motion abnormalities coincided with the area where exercise-induced hypoperfusion was observed with MIBI. CONCLUSIONS: More than a half of syndrome X patients with myocardial perfusion abnormalities also develop regional LV dysfunction during DSE. However, the site of perfusion defects and wall motion abnormalities can be different. Reversible ischemia, defined as a parallel limitation of flow reserve and inducible dysfunction, could be identified as the cause of chest pain in almost one-third of patients.

Adult↗
PubMed2005

Early haemodynamic benefit of sildenafil in patients with coexisting chronic thromboembolic pulmonary hypertension and left ventricular dysfunction.

Sildenafil, a phosphodiesterase type-5 inhibitor, offers potential to treat pulmonary hypertension associated with a variety of conditions. We assessed the early impact of sildenafil on a cohort of patients referred to our unit who had severe pulmonary hypertension secondary to chronic thromboembolic disease which was not amenable to pulmonary thromboendarterectomy and who also had coexisting left ventricular dysfunction. Six patients were studied. Diagnosis of pulmonary embolic disease was made by ventilation perfusion scanning and/or CT pulmonary angiography. All patients were anticoagulated with oral coumarin derivatives and none were considered suitable for pulmonary thromboendarterectomy. Pulmonary hypertension was diagnosed by right heart catheterisation and each patient had Medical Research Council (MRC) dyspnoea score and New York Heart Association (NYHA) class noted and 2D echocardiography prior to commencement of sildenafil 50 mg three times a day. After 6 weeks of sildenafil therapy, right heart catheterisation and 2D echocardiography were repeated, and MRC dyspnoea score, NYHA class and exercise capacity were recorded. All patients demonstrated an improvement in mean pulmonary artery pressure, mean pulmonary capillary wedge pressure, MRC dyspnoea score, NYHA class and gas transfer. No adverse effects of sildenafil were noted. Our data suggests that sildenafil is an effective and well-tolerated therapy for patients with severe pulmonary hypertension associated with pulmonary thromboembolic disease and impaired left ventricular function, producing beneficial effects as early as 6 weeks.

Adult↗
PubMed2002

Microvascular structural correlates of myocardial contrast echocardiography in patients with coronary artery disease and left ventricular dysfunction: implications for the assessment of myocardial hibernation.

BACKGROUND: Myocardial contrast echocardiography (MCE) has been used to evaluate myocardial viability. There are no data, however, on the pathological determinants of myocardial perfusion by MCE in humans and the implications of such determinants. METHODS AND RESULTS: MCE was performed in 20 patients with coronary artery disease and ventricular dysfunction within 24 hours before myocardial biopsy at surgery using a continuous Optison infusion (12 to 16 cc/h), with intermittent pulse inversion harmonics and incremental triggering. Peak myocardial contrast intensity (MCI) and the rate of increase in MCI (beta) were quantitated. Thirty-six transmural myocardial biopsies (2 per patient) were obtained by transesophageal echocardiography. Total microvascular (<100 microm) density, capillary density and area, arteriolar and venular density, and percent collagen content were quantitated with immunohistochemistry. Peak MCI correlated with microvascular density (r=0.59, P<0.001) and capillary area (r=0.64, P<0.001) and inversely correlated with percent collagen content (r=-0.45, P=<0.01). The best relation was observed when the ratio of peak MCI in the 2 biopsied segments in each patient was compared with the ratio of microvascular density and capillary area (r=0.84 and 0.87, respectively; P<0.001). A significant overlap in microvascular density was seen between segments with and without recovery of function. The new MCE indices of blood velocity (beta) and flow (peak MCIxbeta) better identified recovery of function compared with microvascular density and the sole use of peak MCI. CONCLUSIONS: Microvascular integrity is a significant determinant of maximal MCI in humans. MCE indices of blood velocity and flow are important parameters that predict recovery of function after revascularization.

Aged↗
PubMed1997

Severe right ventricular dysfunction following pericardiocentesis for cardiac tamponade.

The accumulation of fluid in the pericardium in an amount sufficient to cause severe obstruction to blood inflow to the ventricles results in cardiac tamponade. In this condition, relief of intrapericardial pressure by pericardiocentesis usually dramatically improves cardiac output, and can be lifesaving. We report a case of a patient with malignant cardiac tamponade in which cardiogenic shock developed after pericardiocentesis due to severe right ventricular dysfunction.

Adenocarcinoma↗
PubMed1999

Prevalence of heart failure and left ventricular dysfunction in the general population; The Rotterdam Study.

AIMS: To determine the prevalence of heart failure and symptomatic as well as asymptomatic left ventricular systolic dysfunction in the general population. METHODS AND RESULTS: In 5540 participants of the Rotterdam Study (age 68.9+/-8.7 years, 2251 men) aged 55-95 years, the presence of heart failure was determined by assessment of symptoms and signs (shortness of breath. ankle oedema and pulmonary crepitations) and use of heart failure medication. In 2267 subjects (age 65.7+/-7.4 years, 1028 men) fractional shortening was measured. The overall prevalence of heart failure was 3.9% (95% CI 3.0+/-4.7) and did not differ between men and women. The prevalence increased with age, with the exception of the highest age group in men. Fractional shortening was higher in women and did not decrease appreciably with age. The prevalence of left ventricular systolic dysfunction (fractional shortening <=25%) was approximately 2.5 times higher in men (5.5%, 95% CI 4.1-7.0) than in women (2.2%, 95% CI 1.4-3.2). Sixty percent of persons with left ventricular systolic dysfunction had no symptoms or signs of heart failure at all. CONCLUSIONS: The prevalence of heart failure is appreciable and does not differ between men and women. The majority of persons with left ventricular systolic dysfunction can be regarded as having asymptomatic left ventricular systolic dysfunction.

Age Factors↗
PubMed1998

Reversible left atrial dysfunction possibly due to afterload mismatch in patients with left ventricular dysfunction.

Limited data are available concerning the influence of altered loading conditions on left atrial (LA) function. In addition, the underlying mechanism of the augmentation of atrial filling (A) velocity (assessed by transmitral Doppler measurement) after treatment of heart failure has been less studied. Therefore, we examined various indexes of LA function during the depression of left ventricular (LV) filling pressure resulting from treatment of heart failure. Twelve patients with LV dysfunction (ejection fraction < 50%) underwent right heart catheterization and transthoracic echocardiography before and after optimal treatment of heart failure. LV/LA volume and ejection fraction and mitral and pulmonary venous flow velocities were measured. LV stiffness (substitute for LA afterload) was assessed by the ratio of LV filling pressure to LV end-diastolic volume. After treatment of heart failure, the mitral A velocity significantly increased (38 +/- 9 to 58 +/- 16 cm/sec, p < 0.005) and there was a distinct attenuation of the difference of the pulmonary venous and mitral A-wave duration (43 +/- 29 to -8 +/- 31 msec, p < 0.005). These findings were associated with a marked decrease in LV stiffness (0.12 +/- 0.04 to 0.05 +/- 0.02 mm Hg/ml, p = 0.0001) and an increase in LA ejection fraction (27% +/- 7% to 38% +/- 8%, p < 0.005). There was a significant curvilinear relation between LA ejection fraction and LV stiffness (r = 0.63, p < 0.01). The mitral A velocity correlated positively with LA ejection fraction (r = 0.77, p < 0.0001) and inversely with LV stiffness (r = -0.52, p < 0.01). The reversible LA dysfunction suggests that the initial LA dysfunction is due to LA afterload mismatch rather than intrinsic LA disease, which also contributes to the augmentation of the mitral A velocity after heart failure treatment.

Atrial Function, Left↗
PubMed2004

Regulation of caspase 3 and Fas in pressure overload-induced left ventricular dysfunction.

BACKGROUND: The presence of apoptotic cell death in cardiac myocytes is now well established and the contribution of apoptosis for the development of heart failure has been suggested. However, the mechanism responsible for the induction of apoptosis remains unclear. The present study was designed to investigate the involvement of Fas and caspase 3 in the transition from pressure overload-induced left ventricular hypertrophy (LVH) to left ventricular dysfunction (LVD). METHODS: Pressure overload induced LVH (10 days) and LVD (30 days) were induced by thoracic aortic banding. Changes in apoptosis-related genes were studied in rats with thoracic aortic banding. After 10 and 30 days, cardiac Fas mRNA expression was measured by RT-PCR. The mRNA expression of caspase 3 was detected by RNase protection assay. The activity of caspase 3 was measured by fluorometric assay. Protein levels of caspase 3 were measured by Western blot. RESULTS: Rats with aortic banding had increased heart/body weight ratios after 10 and 30 days, compared to controls. Central venous pressure and lung weights were increased, left ventricular contractility was significantly impaired only in rats after 30 days of aortic banding, indicating LVD. Caspase 3 mRNA expression (7.1+/-0.1 vs. 2.8+/-0.4, P<0.05), caspase 3 activity (1418+/-181 vs. 849+/-154 AU, P<0.05) as well as caspase 3 protein levels were increased in rats with LVD but not with LVH. Similarly, Fas mRNA was increased in rats with LVD. CONCLUSIONS: The activation of Fas and caspase 3 only after 30 days of aortic banding suggests that induction of these pathways may be involved in pressure overload-induced LVD.

Animals↗
PubMed2004

Evaluation of right ventricular dysfunction in patients with cardiac amyloidosis using Tei index.

BACKGROUND: Cardiac amyloidosis is an infiltrative disease causing predominant diastolic dysfunction and systolic dysfunction at its advanced stage. Right ventricular (RV) dysfunction is an independent predictor of poor prognosis in congestive heart failure and cardiomyopathies. However, the assessment of RV function is still technically difficult because of the complicated geometry of the RV. The recently proposed Tei index, obtained from the cardiac time interval analysis, allows noninvasive and quantitative estimation of global ventricular function without geometric evaluation. Therefore, this study was designed to assess RV function for patients with cardiac amyloidosis. METHODS: Study patients consisted of 30 consecutive patients with biopsy specimen-proven cardiac amyloidosis and 50 control subjects. Patients were classified as having early or advanced stage of cardiac amyloidosis on the basis of mean left ventricular wall thickness < 15 mm or >/= 15 mm. Tei index, defined as the sum of isovolumetric contraction and relaxation time divided by ejection time, was obtained from tricuspid and pulmonary Doppler flow velocity. RESULTS: RV Tei index was significantly increased for patients with cardiac amyloidosis (0.54 +/- 0.16 vs 0.28 +/- 0.05, amyloidosis vs control, P <.001). The incidences of abnormal RV isovolumetric contraction time, ejection time, isovolumetric relaxation time, and Tei index in all patients with cardiac amyloidosis were 63%, 43%, 73%, and 83%, respectively. The same incidences were 50%, 13%, 63%, and 75% in the early stage and 68%, 54%, 77%, and 86% in the advanced stage, respectively. CONCLUSION: Patients with cardiac amyloidosis frequently have RV dysfunction even in its early stage. Tei index allows simple, noninvasive, and nongeometric estimation of RV dysfunction in patients with cardiac amyloidosis.

Adult↗
PubMed2005

Reversible ventricular dysfunction takotsubo cardiomyopathy.

BACKGROUND: Recently, many cardiologists have recognized the existence of a rapidly reversible form of heart failure of unknown origin characterized by a takotsubo-shaped, dyskinetic left ventricle on left ventriculography. AIM: To determine the detailed clinical features of takotsubo cardiomyopathy. METHODS: Thirteen elderly patients (11 women and 2 men with a mean age of 75.3 years) who had normal coronary arteries and takotsubo-like left ventricular dysfunction were prospectively enrolled in this study. RESULTS: Cardiac enzymes did not increase significantly, but the mean plasma norepinephrine level was very high on admission (0.98 microg/l). Coronary angiography revealed normal coronary arteries in all patients, but left ventriculography showed apical akinesis combined with basal hyperkinesis, i.e., a takotsubo (Japanese octopus fishing pot)-shaped ventricle. Left ventricular wall motion normalized within a mean of 16.9 hospital days in 12 patients, but 1 patient died of acute renal failure on hospital day 7. Cardiac events did not recur during a follow-up period of 0.5 to 5 years. CONCLUSION: Takotsubo cardiomyopathy seems to be a new type of acute heart failure, which generally has a good prognosis and does not recur. Myocardial damage by catecholamine overload, adrenoceptor hypersensitivity, and changes of catecholamine dynamics due to stress may cause this condition.

Aged↗
PubMed1993

Markers of left ventricular dysfunction induced by exercise, dipyridamole or combined stress on ECG-gated myocardial perfusion scans.

An index of left ventricular contraction can be extracted from the cavitary time-activity curve of electrocardiographic (ECG)-gated myocardial perfusion scans. To assess the induction of stress-induced myocardial depression, we compared contraction indexes derived from immediate poststress and delayed 201Tl images with indexes of ventricular dilation and lung uptake in the prediction of severe coronary artery disease (defined as two or more 90% stenoses). Stress procedures were performed in 93 patients with symptom-limited supine bicycle exercise alone, and in 227 with intravenous dipyridamole, combined where possible with exercise. The immediate and delayed contraction indexes reflected left ventricular dysfunction on ventriculography (P < 0.0001), but additionally the immediate index was reduced (P < 0.0001) in severe coronary disease. Stress-induced hypokinesis was seen frequently after each of the test modes. The relationship with angiographic findings was better defined for indexes of contraction than for lung uptake or ventricular dilation (P < 0.01). The prediction of severe coronary disease was optimized by combining the poststress contraction index and lung uptake. These data support the use of ECG-gated myocardial scans in evaluating the functional consequences of stress/imaging procedures.

Biomarkers↗