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At least 289 records · Page 16Linked to original sources
PubMed2004

High prevalence of right ventricular systolic dysfunction in early systemic sclerosis.

OBJECTIVE: To assess right ventricular (RV) function in patients with early systemic sclerosis (SSc) and the acute effects of calcium channel blockers on RV ejection fraction (RVEF). METHODS: Forty-two consecutive patients with SSc with less than 5 years' disease duration and normal pulmonary arterial pressure (35 women, 7 men; mean age 54.3 +/- 9.7 years; 16 with diffuse and 26 with limited cutaneous forms, systolic pulmonary arterial pressure 30.3 +/- 5.4 mmHg) were prospectively evaluated. All underwent pulmonary function testing, echocardiography, and radionuclide ventriculography at rest and 2 hours after receiving 40 mg oral nicardipine, and were compared at baseline with 20 gender and age matched controls. RESULTS: None of the patients with SSc had clinical evidence of heart failure. At baseline, SSc patients had significantly lower LVEF (68.5% +/- 7.9 vs 72.4% +/- 5.0, p = 0.049) and RVEF (36.5% +/- 7.0 vs 45.8% +/- 5.7, p < 0.0001). Sixteen patients had reduced RVEF (< 35%), 3 had reduced LVEF (< 55%), and 10 had reduced peak filling rate (PFR). RVEF correlated to both LVEF and PFR (r = 0.64, p < 0.0001, and r = 0.36, p = 0.0037, respectively), whereas no correlation was found with pulmonary function impairment or pulmonary arterial pressure. Nicardipine resulted in a significant increase in RVEF (from 36.5% +/- 7.0 to 42.3% +/- 8.4, p < 0.001) whereas afterload indicated by mean arterial pressure did not differ significantly. CONCLUSION: Reduced RVEF appears to be a common feature in early SSc; it may be due to intrinsic myocardial involvement and is acutely improved by nicardipine.

Adult↗
PubMed2006

[Persistent left ventricular systolic dysfunction in a patient with ampulla cardiomyopathy: a case report].

An 81-year-old woman was admitted for treatment of diastolic heart failure. Two weeks after admission, she suffered sudden chest pain without somatic and/or psychological stress. Electrocardiography showed ST elevation in leads V2- V5. Coronary angiography did not reveal any significant stenosis in the epicardial coronary artery. Left ventriculography showed apical akinesis with basal and mid hyperkinesis. The diagnosis was ampulla cardiomyopathy. The abnormality on electrocardiography was normalized 2 months later, but apical akinesis persisted for 1 year. Myocardial contrast echocardiography showed microvascular dysfunction consistent with the apical akinesis for 1 year. Microvascular dysfunction may be important in the pathophysiological state of ampulla cardiomyopathy.

Aged, 80 and over↗
PubMed2000

Regional patterns of left ventricular systolic dysfunction after subarachnoid hemorrhage: evidence for neurally mediated cardiac injury.

Although left ventricular (LV) dysfunction has been described after subarachnoid hemorrhage (SAH), its pathophysiology, regional distribution, and reversibility remain uncertain. To test the hypothesis that regional wall motion patterns in SAH patients do not match the typical patterns observed in coronary artery disease, a segmental wall motion analysis was performed in 30 SAH patients with LV dysfunction. Both regional (n = 21) and global (n = 9) wall motion patterns were observed. Preservation of apical function relative to the base was observed in 17 (57%) of the 30 patients. Many of the wall motion patterns were atypical of coronary artery disease but correlated with the distribution of the myocardial sympathetic nerve terminals. Five subjects had follow-up echocardiograms with resolution of LV dysfunction in all cases. In conclusion, a previously unreported, apex-sparing pattern of LV dysfunction is described, providing indirect evidence for a neurally mediated mechanism of cardiac injury. Limited data indicate that LV dysfunction in SAH patients is potentially reversible.

Acute Disease↗
PubMed2006

Left ventricular systolic dysfunction and the risk of ischemic stroke in a multiethnic population.

BACKGROUND AND PURPOSE: Left ventricular dysfunction (LVD) is associated with cardiovascular mortality. Its association with ischemic stroke has been mainly documented after myocardial infarction. The stroke risk associated with LVD, especially of mild degree, in the general population is unclear. The purpose of this study was to evaluate the relationship between LVD and ischemic stroke in a multiethnic cohort. METHODS: LV systolic function was assessed by transthoracic 2-dimensional echocardiography in a subset of subjects from the Northern Manhattan Study (NOMAS), 270 patients with first ischemic stroke and 288 age-, gender- and race-matched community controls. LV ejection fraction was measured by a simplified cylinder-hemiellipsoid formula, and categorized as normal (>50%), mildly (41% to 50%), moderately (31% to 40%) or severely (< or =30%) decreased. The association between impaired ejection fraction and ischemic stroke was evaluated by logistic regression analysis after adjustment for established stroke risk factors. RESULTS: LVD of any degree was more frequent in stroke patients (24.1%) than in controls (4.9%; P<0.0001), as was moderate/severe LVD (13.3% versus 2.4%; P<0.001). A decreased ejection fraction was associated with ischemic stroke even after adjusting for other stroke risk factors. The adjusted odds ratio for any degree of LVD was 3.92 (95% CI, 1.93 to 7.97). The adjusted odds ratio for mild LVD was 3.96 (95% CI, 1.56 to 10.01) and for moderate/severe LVD 3.88 (95% CI, 1.45 to 10.39). The association between LVD of any degree and stroke was present in all age, gender and race-ethnicity subgroups. CONCLUSIONS: LVD, even of mild degree, is independently associated with an increased risk of ischemic stroke. The assessment of LV function should be considered in the assessment of the stroke risk.

Adult↗
PubMed1997

The effects of pathophysiological increments in brain natriuretic peptide in left ventricular systolic dysfunction.

Plasma levels of brain natriuretic peptide (BNP) are raised in patients with left ventricular impairment and may play a role in the adaptation to left ventricular impairment. Manipulation of BNP levels may have therapeutic potential. The effects of BNP have not been well studied in patients with left ventricular impairment. We studied the effects of low-dose BNP infusion, reproducing the increment in plasma BNP seen with progression from mild to severe heart failure in patients with impaired left ventricular systolic function. BNP was infused in a placebo-controlled, single-blind, crossover design at a rate of 3.3 pmol x kg(-1) x min(-1) over 4 hours to 8 patients with a history of congestive heart failure and persistent impairment of left ventricular systolic function (left ventricular ejection fraction <35%). Endocrine, renal, and hemodynamic effects were measured. Compared with time-matched placebo-control, BNP infusion decreased mean systemic arterial pressure (peak decrease, 17.1 mm Hg; P=.04), mean pulmonary artery pressure (peak decrease, 6.1 mm Hg; P=.007), mean pulmonary capillary wedge pressure (peak decrease, 5.5 mm Hg; P=.04), and systemic vascular resistance (peak decrease, 1400 dyne s(-1) cm(-5); P=.015), but cardiac output and heart rate were unchanged. Urinary volume and urinary excretion of sodium and potassium were not altered. BNP infusion increased plasma cGMP (2.3-fold change, P=.002). Plasma atrial natriuretic peptide levels were increased for the first hour of BNP infusion (peak increase, 11.5 pmol/L; P=.005). Plasma aldosterone levels were unchanged during but increased over time-matched control levels after the end of the BNP infusion (peak increase, 90 pmol/L; P=.02). Plasma renin activity and cortisol and catecholamine levels were unchanged. Low-dose infusion of BNP causes favorable hemodynamic changes and relative neurohormonal suppression but has attenuated renal effects in patients with impaired left ventricular systolic function.

Aged↗
PubMed2000

Diuretic therapy in elderly heart failure patients with and without left ventricular systolic dysfunction.

Long term prescription of diuretics for heart failure is very prevalent among elderly patients, although the rationale for such a treatment strategy is often unclear, as diuretics are not indicated if volume overload is absent. The concept of diastolic heart failure in the elderly might particularly change the role of diuretic therapy, since diuretics may have additional adverse effects in these patients. This paper reviews the effects of diuretic therapy in elderly patients with heart failure, emphasising the differences between patients with normal and decreased left ventricular systolic function. Studies on diuretic withdrawal in elderly patients with heart failure are discussed, with emphasis on issues involved in decision making such as diuretic dose reduction and withdrawal in elderly patients and factors that have been established to predict successful withdrawal. Existing guidelines on the prescription of diuretics in elderly patients with heart failure with normal and decreased left ventricular systolic function and in those with diastolic heart failure are also discussed. By reducing intravascular volume, diuretics may further impair ventricular diastolic filling in patients with diastolic heart failure and thus reduce stroke volume. Indeed, preliminary studies demonstrate that diuretics may provoke or aggravate hypotension on standing and after meals in these patients. Therefore, it is suggested that elderly patients with heart failure with intact left ventricular systolic function should not receive long term diuretic therapy, unless proven necessary to treat or prevent congestive heart failure. This implies that physicians should carefully evaluate the opportunities for diuretic dose tapering or withdrawal in all of these patients, and that a cautiously guided intermittent diuretic treatment modality may be critical in the care for older patients with heart failure with intact left ventricular systolic function.

Aged↗
PubMed2001

Reversible left ventricular systolic dysfunction--reversibility of coronary microvascular abnormality.

Reversible left ventricular wall motion abnormalities mimicking myocardial infarction have been reported in patients with a noncardiac illness. Their coronary angiograms do not demonstrate organic stenosis or epicardial coronary vasospasm. In this article, two cases of reversible left ventricular contraction abnormality are presented. Electrocardiography showed deep inverted T waves in precordial leads, and the echocardiography revealed diffuse akinesis of the apical region in the acute phase. Coronary angiography showed no significant stenosis or occlusion in either patient. Thallium scintigraphy showed no defect, while the metaiodobenzylguanidine scintigraphy demonstrated significant defects in the apex. The relative coronary flow reserve ratio, measured with an intracoronary Doppler flow wire, was significantly reduced in both patients. Myocardial contrast echocardiography revealed a reversible perfusion defect in the apex in the acute phase in case 2. Transiently impaired coronary microcirculation was thought to be involved in the pathogenesis of the reversible left ventricular dysfunction observed in these patients.

Aged↗
PubMed1996

Comparison of atrial natriuretic peptide B-type natriuretic peptide, and N-terminal proatrial natriuretic peptide as indicators of left ventricular systolic dysfunction.

We have directly compared atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and N-terminal pro-ANP (N-ANP) as markers of patients with left ventricular ejection fraction (LVEF) < or = 35%, as measured by radionuclide ventriculography. Venous blood samples were obtained from an unselected group of 87 patients who had been referred for assessment of ventricular function. ANP, BNP, and N-ANP were measured by radioimmunoassay using commercial kits. Receiver-operating characteristic analysis was used for the objective assessment of the diagnostic performance of each assay. There was a weak negative correlation between LVEF and plasma levels of ANP-li (r = -0.50,), BNP-li (r = -0.57), and N-ANP-li (r = -0.49) (p <0.01 for each peptide). Areas under the receiver-operating characteristic curves for BNP (0.880) and N-ANP (0.832) were not significantly different from each other, but were both significantly greater than the value for ANP (0.761): BNP versus ANP, p <0.01; and N-ANP versus ANP, p <0.05. The optimal sensitivity and specificity of each assay for the detection of patients with LVEF < or = 35% were: BNP > 4 pmol/L-sensitivity 1.0, specificity 0.58; N-ANP >200 pmol/L-sensitivity 0.95, specificity 0.35; and ANP >10 pmol/L-sensitivity 0.90, specificity 0.30. Plasma concentrations of BNP and N-ANP provide sensitive indicators of moderate to severe LV dysfunction; both peptides, are objectively superior to ANP for identifying patients with LVEF < or = 35%. These simple tests could be used to screen patients with suspected ventricular dysfunction to reduce the demand for further cardiac investigations.

Aged↗
PubMed1997

Isolated myocyte contractile function is normal in postinfarct remodeled rat heart with systolic dysfunction.

BACKGROUND: Postinfarction ventricular remodeling is associated with lengthening and contractile dysfunction of the remote noninfarcted myocardium. Mechanisms underlying this phenomenon remain unclear. METHODS AND RESULTS: We studied serial changes in global left ventricular (LV) structure and function in infarcted (1, 2, 4, and 6 weeks after myocardial infarction) and sham-operated rat hearts and correlated them with structural and functional changes in myocytes isolated from the remote LV myocardium in the same hearts. Rats with myocardial infarction developed significant remodeling. The heart weight-to-body weight ratios were increased. LV volumes at filling pressure of 10 mm Hg were higher (305+/-28 versus 215+/-12 microL, P<.01). This was accompanied by global LV dysfunction (in vivo LV end-diastolic pressure, 4+/-1 versus 23+/-1.6 mm Hg; Langendorff LV developed pressure, 105+/-4 versus 62+/-9 mm Hg, P<.001 for both). Myocytes isolated from these hearts showed significant structural remodeling (LV myocytes, 24% longer and 15% wider; right ventricular myocytes, 38% longer and 31% wider, all P<.05). LV myocyte length correlated with changes in LV volume (r=.79) and function (LV developed pressure, r=-.81). However, LV myocytes from the same hearts showed normal contractile function and intracellular Ca2+ transients at baseline and during inotropic stimulation with increasing extracellular Ca2+ (1 to 6 mmol/L). The shortening-frequency relationship was also similar in myocytes from sham and myocardial infarction rats. CONCLUSIONS: Postinfarct LV remodeling occurs predominantly by myocyte lengthening rather than by myocyte slippage. However, contractile function of the unloaded myocytes from the remote noninfarcted LV myocardium of the remodeled heart is normal. Therefore, myocyte contractile abnormalities may not contribute to global dysfunction of the remodeled heart. Reduced myocyte mass and nonmyocyte factors like increased wall stress, altered LV geometry, and changes in the myocardial interstitium may be more important in the genesis of postinfarct LV dysfunction in this model.

Animals↗