Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Systolic 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.

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

At least 1,279 records · Page 71Linked to original sources
PubMed2001

Changes in calcium cycling precede cardiac dysfunction during autoimmune myocarditis in mice.

Myocardial inflammation contributes to the development of dilated cardiomyopathy, as well as other cardiac diseases. We have previously shown decreased left ventricular function in mice with autoimmune myocarditis. To test the hypothesis that decreased function is mediated by changes in contractility and/or Ca2+ cycling, we isolated cardiac myocytes from mice with myocarditis and age-matched controls at two time points: day 18 (prior to cardiac dysfunction) and day 35 (during cardiac dysfunction). We measured cell shortening and the Ca2+ transient simultaneously at 28 degrees C and 0.3 Hz. We also quantified proteins which regulate contractility and [Ca2+](i), using Western blot analysis. Results showed no change in cell shortening or systolic Ca2+ on day 18, despite a significant reduction in diastolic Ca2+. By day 35, the decrease in diastolic Ca2+ was accompanied by significantly reduced cell shortening and a decrease in the systolic Ca2+ transient. Protein levels of the sarcoplasmic reticulum Ca2+ ATPase were unchanged at both time points, while phospholamban and the sodium/calcium exchanger were significantly reduced in myosin-immunized mice at both time points. Calsequestrin was unchanged at day 18, but was significantly reduced in the myosin-immunized mice on day 35. Results of this study suggest that decreased diastolic Ca2+, as well as protein levels of phospholamban and the sodium/calcium exchanger, may actually contribute to disease progression in autoimmune myocarditis, while changes in calsequestrin may be related to systolic dysfunction in this model.

Animals↗
PubMed2004

Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-B pathway.

OBJECTIVES: We sought to clarify that a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activator inhibits myocardial fibrosis and its resultant diastolic dysfunction in hypertensive heart disease, as well as to investigate whether inflammatory mediators through the nuclear factor (NF)-kappa-B pathway are involved in the effects. BACKGROUND: Patients with hypertensive heart disease often have diastolic heart failure without systolic dysfunction. Meanwhile, it has been well established in atherosclerosis that PPAR-alpha activation negatively regulates early inflammation. In hypertensive hearts, however, it is still unclear whether PPAR-alpha activation inhibits inflammation and fibrosis. METHODS: Twenty-one rats were randomly separated into the following three groups: deoxycorticosterone acetate (DOCA)-salt hypertensive rats treated with a PPAR-alpha activator, fenofibrate (80 mg/kg/day for 5 weeks); DOCA-salt rats treated with vehicle only; and uni-nephrectomized rats as normotensive controls. RESULTS: Fenofibrate significantly inhibited the elevation of left ventricular end-diastolic pressure and the reduction of the magnitude of the negative maximum rate of left ventricular pressure rise and decline, corrected by left ventricular pressure (-dP/dt(max)/P), which are indicators of diastolic dysfunction. Next, fenofibrate prevented myocardial fibrosis and reduced the hydroxyproline content and procollagen I and III messenger ribonucleic acid expression. Finally, inflammatory gene expression associated with NF-kappa-B (interleukin-6, cyclooxygenase-2, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1), which is upregulated in DOCA-salt rats, was significantly suppressed by fenofibrate. Activation of NF-kappa-B and expression of I-kappa-B-alpha in DOCA-salt rats were normalized by fenofibrate. CONCLUSIONS: A PPAR-alpha activator reduced myocardial fibrosis and prevented the development of diastolic dysfunction in DOCA-salt rats. The effects of a PPAR-alpha activator may be mediated partly by prevention of inflammatory mediators through the NF-kappa-B pathway. These results suggest that treatment with PPAR-alpha activators will improve diastolic dysfunction in hypertensive heart disease.

Animals↗
PubMed1989

Can prognosis be altered by treating LV dysfunction?

A major scientific effort taking place in the last decade has resulted in better understanding of the pathophysiology of myocardial dysfunction and in the development of new therapeutic modalities for this condition. The purpose of this article is to review available information related to the effect of available therapeutic modalities on mortality rate in patients with left ventricular (LV) systolic dysfunction.

Adrenergic alpha-Antagonists↗
PubMed2002

[Myocardial and coronary vessel dysfunction in diabetes I patients].

Despite of dramatic improvement in diagnostic procedures and treatment of diabetic patients, cardio-vascular complications are still the most frequent causes of death in these patients. Diabetes influences myocardial and coronary vessels function by coexisting macroangiopathy, microangiopathy, metabolic disturbances and autonomic nervous system neuropathy. All these factors result in diastolic and systolic dysfunction of the heart. Cardiomyopathy, congestive heart failure and serious arrhythmias are the end stage of diabetic complications. Macroangiopathy demonstrates accelerated atherosclerosis (involving coronary arteries), which consequences can be observed in 1 type diabetes patients at around the age of 30. Causes of increased risk of macroangiopathy in type 1 diabetic patients are not clear. There are not many clinical, prospective trials which can allow for etiology determination of the increased incidence of atherosclerosis and mortality due to coronary artery disease in this population. Adding to traditional risk factors of atherosclerosis like genetic factors, hypertension, dyslipidemia, obesity, smoking and improper diet, other important risk factors are observed in diabetic patients. Only few clinical trials suggest that hyperglycemia, glycation, glycoxidation of proteins, lipoproteins, changes in their composition, microalbuminuria, coagulation, fibrinolytic disturbances are additional risk factors of endothelium dysfunction and atherosclerosis. Prevention and treatment of accelerated coronary artery disease and it's consequences are more complicated in the diabetic population than in others. Some of the clinical trials suggest that even improved glycemic control does not eliminate the elevated risk of coronary artery disease in type 1 diabetic patients.

Arrhythmias, Cardiac↗
PubMed2005

Neurohormonal activation and diagnostic value of cardiac peptides in patients with suspected mild heart failure.

BACKGROUND: Data describing activation of brain natriuretic peptide (BNP) system relative to the renin-angiotensin-aldosterone system (RAAS) are sparse in the early phase of heart failure (HF). AIMS: To compare activation of BNP system relative to RAAS hyperactivity and to assess diagnostic accuracy of cardiac peptides to detect any left ventricular dysfunction (LVD) in patients referred from primary care with suspected HF before institution of medical therapy. METHODS: Of 166 referred patients 150 were consecutively included (14 were excluded and two refused consent). Echocardiography and measurements of neurohormonal activity were performed. Systolic dysfunction (LVSD) was defined as an ejection fraction<or=0.45. Abnormal left ventricular filling was determined by a combination of Doppler techniques. RESULTS: LVSD with concomitant abnormal left ventricular filling was present in 22 patients, and abnormalities in left ventricular filling alone were present in 58. Median BNP were 307 and 37 pg/ml while median N-terminal proBNP (NT-proBNP) were 2285 and 199 pg/ml in the two groups respectively, and were significantly lower in patients without LVD (BNP: 8 pg/ml and NT-proBNP: 55 pg/ml, P<0.0001). NT-proBNP demonstrated a weak negative correlation with renin (r=-0.18, P=0.03) and aldosterone (r=-0.18, P=0.03), but no significant correlation with Ang II (r=-0.14, P=0.10) or noradrenaline (r=0.11, P=0.19). Renin correlated well with Ang II (r=0.85, P<0.0001), and aldosterone (r=0.41, P<0.0001). RAAS and noradrenaline demonstrated no diagnostic potential for the diagnosis of any LVD with areas under ROC curves close to 0.50. The area was 0.93 (95% CI 0.90-0.98) for BNP and 0.95 (0.91-0.99) for NT-proBNP. In 5-10% of patients with LVD, BNP and NT-proBNP were under the selected thresholds. CONCLUSION: Patients with LVD demonstrated considerable activation of the BNP system, whereas RAAS hyperactivity could not be demonstrated. Thus, BNP and NT-proBNP had a considerable diagnostic potential even in patients with mild HF.

Adult↗
PubMed2006

Changes in connexin 43, metalloproteinase and tissue inhibitor of metalloproteinase during tachycardia-induced cardiomyopathy in dogs.

OBJECTIVE: To study changes in connexin, metalloproteinase and tissue inhibitor of metalloproteinase levels during tachycardia-induced cardiomyopathy (TIC). METHODS: Canine models of TIC were established by rapid right atrial pacing at 350-400 beats per min for 8 weeks in 11 dogs, six dogs acted as a sham operation group. Echocardiography, left ventricular pressure and its first derivation with time (positive and negative maximum, dp/dtmax, -dp/dtmax), and intracardiac electrograms were recorded before and after rapid pacing at 1, 4 and 8 weeks. Data were acquired in sinus rhythm. Ultrastructural changes in left ventricular tissue were observed by transmission electron microscope. Connexin 43 (Cx43) levels in the left ventricular myocardium were measured by confocal laser microscopy. The relative abundance of matrix metalloproteinase (MMP-2) and tissue inhibitor of metalloproteinase (TIMP-2) were studied by immunoblotting. RESULT AND CONCLUSIONS: (1) Ventricular dilatation and systolic dysfunction occurred after 1 week of rapid right atrial pacing. (2) There was structural damage to the myofibrils, mitochondria, and the sarcoplasmic reticulum with intercalated disk discontinuity. (3) Levels of Cx43 decreased significantly and gap junction remodelling occurred during TIC. (4) TIC may result from several mechanisms, such as ultrastructural changes or gap junction and matrix remodelling.

Animals↗
PubMed2003

Antiremodeling effect of long-term exercise training in patients with stable chronic heart failure: results of the Exercise in Left Ventricular Dysfunction and Chronic Heart Failure (ELVD-CHF) Trial.

BACKGROUND: The effects of exercise training (ET) on left ventricular (LV) remodeling in chronic heart failure are not definitively established, and the safety of ET in these patients is still debated. METHODS AND RESULTS: This multicenter study investigated the long-term effect of moderate ET on LV remodeling, work capacity, and quality of life (QoL) in 90 patients with stable chronic heart failure caused by LV systolic dysfunction, randomized to a 6-month ET program (T, n=45) or a control group (C, n=45). All patients underwent resting echocardiography, a cardiopulmonary exercise test, 6-minute walking test, and QoL assessment at entry and after 6 months. At entry, end-diastolic (EDV) and end-systolic (ESV) volume, ejection fraction, work capacity, peak o2, and walking distance were similar in the 2 groups. After 6 months, LV volumes diminished in T (EDV, from 142+/-26 to 135+/-26 mL/m2, P<0.006; ESV, from 107+/-24 to 97+/-24 mL/m2, P<0.05) but increased in C (EDV, from 147+/-41 to 156+/-42 mL/m2, P<0.01; ESV, from 110+/-34 to 118+/-34 mL/m2, P<0.01). Ejection fraction improved in T (P<0.001) but was unchanged in C (P=NS). Significant improvement in work capacity (P<0.001), peak VO2 (P<0.006), walking distance (P<0.001), and QoL (P<0.01) was observed in T but not in C (P=NS). T showed a trend toward fewer (P=0.05) hospital readmissions for worsening dyspnea in the absence of other adverse cardiac events. CONCLUSIONS: In stable chronic heart failure, long-term moderate ET has no detrimental effect on LV volumes and function; rather, it attenuates abnormal remodeling. Furthermore, ET is safe and effective in improving exercise tolerance and QoL.

Cardiac Volume↗
PubMed2005

Influence of angiotensin II receptors blocking on overall left ventricle's performance of patients with acute myocardial infarction of limited extent. Echocardiographic assessment.

INTRODUCTION: Recent studies documented the beneficial effect of angiotensin-receptor blockers (ARBs) on patients (pts) with acute myocardial infarction (AMI) combined with left ventricle (LV) systolic dysfunction. The present study intended to assess the impact of the ARB irbesartan, on the overall LV performance in pts with uncomplicated AMI of limited extent. METHODS: Forty consecutive pts with first inferior AMI (AMI-I) and preserved LV-systolic function were enrolled. They were allocated into two groups: (a) 20 pts received the conventional treatment of AMI-I and placebo (CT) and (b) 20 pts administered irbesartan additionally to the conventional treatment (IR). Twenty four healthy individuals of matching age and sex were recruited as control group (CG). Complete echocardiographic examination, Tei index of overall LV function and systolic blood pressure (SBP) were measured on the 8th post-infarct day. RESULTS: The Tei index of IR group (0.53+/-0.03) was significantly lower compared to that of CT group (0.78+/-0.05) (p<0.001) and was similar to that of CG (0.45+/-0.03)(p=NS). Irbesartan induced a considerable decrease in both isovolumic relaxation (115+/-7 ms vs 140+/-7 ms; p<0.01) and contraction time (52+/-2 ms vs 64+/-3 ms; p<0.01) and a significant increase in ejection time (279+/-6 ms vs 256+/-8 ms; p<0.05). SBP in pts of IR group was similar to that of CT group (112+/-3 mmHg vs 113+/-4 mmHg; p=NS). CONCLUSIONS: Therapy with Irbesartan improves overall LV function of pts with AMI-I. Irbesartan leads to acceleration of the LV relaxation, which possibly indirectly ameliorates LV systolic performance too. This beneficial influence is possible attributed to a direct tissue effect of the drug and not to its hemodynamic action.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Use of strain and tissue velocity imaging for early detection of regional myocardial dysfunction in patients with beta thalassemia.

BACKGROUND AND AIM OF STUDY: Iron overload contributes to cardiac dysfunction in patients with beta thalassemia (Th). Tissue velocity and strain imaging (TVI and SI) might prove useful in early detection of regional myocardial dysfunction in these patients. The aim of this study is to clarify the value of TVI and SI in early detection of regional myocardial dysfunction in thalassemia patients. METHODS AND RESULTS: This study included two age-matched groups; G1: 27 Th patients and G2: 14 normal subjects. Conventional echo-Doppler measures of LV and RV dimensions and function were obtained. TVI measures included systolic and diastolic myocardial velocities (Sm, Em, Am and Em/Am) of the basal segments of septal wall, lateral LV and RV free walls. Systolic strain values were measured in the same basal segments and included S-septal, S-LV and S-RV. Strain and TVI data were compared in the two groups. Sm and strain values were compared in the different walls (LV, RV and septum) in each group separately. S-LV was lower in G1 than G2 (20.9 +/- 6.8 vs 27.2 +/- 4.3, p < 0.001), while S-septal was higher in G1 than G2 (31.1 +/- 8.3 vs 25.1 +/- 3.8, p < 0.01). TVI measures of diastolic performance of the septal and RV walls were different in G1 compared to G2. Septal-Em was lower, septal-Am was higher and septal-Em/Am was lower in G1 compared to G2. RV-Am was higher and RV-Em/Am was lower in G1 compared to G2. Other SI and TVI measures were not significantly different in G1 from G2. Sm and strain values were lower in the lateral LV wall compared to septal wall in G1 but not in G2, while the corresponding values of the RV wall were higher than those of the septal and LV walls in both groups (G1 and G2). CONCLUSION: Thalassemia patients have regional systolic dysfunction in the lateral LV wall and regional diastolic dysfunction in the septal and RV wall. TVI and the newer modality SI are promising tools for quantitative assessment of regional myocardial function. SI seems more capable of early detection of regional myocardial dysfunction.

Adolescent↗
PubMed1997

Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies.

The increasing prevalence of congestive heart failure has focused importance on the search for potentially reversible etiologies of cardiomyopathy. The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both animal models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm control. Sustained rapid pacing in experimental animal models can produce severe biventricular systolic dysfunction. Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in ventricular function for up to 3 to 5 weeks, resulting in end-stage heart failure. The recovery from pacing-induced cardiomyopathy demonstrates that the myopathic process associated with rapid heart rates is largely reversible. Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fraction shows significant recovery with subsequent normalization after 1 to 2 weeks. In humans, descriptions of reversal of cardiomyopathy with rate or rhythm control of incessant or chronic tachycardias have been reported with atrial tachycardias, accessory pathway reciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid ventricular responses. Control of AF rapid ventricular responses has been demonstrated to improve ventricular dysfunction with cardioversion to sinus rhythm, pharmacologic ventricular rate control and AV junction ablation and permanent ventricular pacing. The investigation of potential tachycardia-induced cardiomyopathy in patients with heart failure requires further prospective confirmation in larger numbers of patients, with study of mechanisms, patient groups affected and optimal therapies.

Animals↗
PubMed2004

Endothelial dysfunction and damage in congestive heart failure: relation of flow-mediated dilation to circulating endothelial cells, plasma indexes of endothelial damage, and brain natriuretic peptide.

BACKGROUND: Congestive heart failure (CHF) is associated with endothelial perturbation (as defined by flow-mediated endothelial-dependent vasodilation [FMD, an index of endothelial dysfunction], circulating endothelial cells [CECs, an index of endothelial damage], or plasma indexes of endothelial damage/dysfunction [eg, von Willebrand factor (vWf) and soluble thrombomodulin (sTM)]) and raised plasma levels of brain natriuretic peptide (BNP, a peptide hormone associated with left ventricular systolic dysfunction and prognosis). However, the relations between these parameters are unclear. METHODS AND RESULTS: To test the hypothesis that there is a relation between endothelial perturbation (defined by FMD, CECs, vWf, and sTM) and BNP in CHF, we studied these indexes in 30 patients with CHF who were compared with 20 age-matched control subjects. FMD, CECs, plasma vWf, and BNP levels (but not sTM) were all abnormal in patients with CHF. There were significant inverse correlations between FMD and vWf (P=0.001), CECs (P=0.002) and BNP (P=0.006) as well as a positive correlation between CECs and vWf (P=0.032). In multivariate analysis, BNP (P<0.001) and FMD (P<0.001) were both independently associated with CHF. CONCLUSIONS: Ample evidence of endothelial cell damage/dysfunction in CHF cannot be fully explained by the variance in plasma BNP per se. Therefore, the routes by which these indexes influence the pathophysiology of CHF as well as predict adverse outcomes may be independent.

Aged↗
PubMedDate not supplied

Biocompatibility of heparin-coated cardiopulmonary bypass circuits in coronary patients with left ventricular dysfunction is superior to PMEA-coated circuits.

BACKGROUND: Several coating techniques for extracorporeal circulation have been developed to diminish the systemic inflammatory response during cardiopulmonary bypass (CPB). The aim of this study was to evaluate the clinical effectiveness and biocompatibility of heparin-coated and poly-2-methoxyethylacrylate (PMEA)-coated CPB circuits on coronary patients with left ventricular systolic dysfunction. METHODS: Thirty-six patients who underwent elective coronary artery bypass grafting were divided into two equal groups: group H (n = 18), heparin-coated; group P (n = 18), PMEA coated. Clinical outcomes, hematologic variables, cardiac enzymes, malondialdehyde (MDA), and acute phase inflammatory response (including myeloperoxidase (MPO), catalase, hsCRP, and IL-8) were analyzed perioperatively. RESULTS: Demographic, CPB, and clinical outcome data were similar for both groups. Plasma fibrinogen, total protein, albumin, and platelet count decreased, neutrophil count, MDA, IL-8, MPO, and catalase levels increased during CPB. During CPB, MPO and catalase values were significantly higher in group P (p = 0.02 and p = 0.01) and postoperative MDA concentration was lower in group H (p = 0.03). Platelet counts were better preserved in group H during and after CPB but neutrophil count and IL-8 level did not differ between the groups. Postoperative total protein, albumin, and fibrinogen levels were higher in group H (p < 0.05). The postoperative first day levels of troponin-I, CK-MB, and CRP increased in both groups without any significant differences between the groups. CONCLUSIONS: Heparin-coated circuit provided better suppression of perioperative inflammatory markers and exhibited more favorable effects on hematologic variables than PMEA-coated circuit.

Acrylates↗
PubMedDate not supplied

Diastolic dysfunction in arterial hypertension.

Left ventricular diastolic properties are important markers of pump function and are frequently abnormal when myocardial insults alter tissue structure. Alterations can be limited to the early diastolic phase (early active relaxation) or to late diastolic filling (late ventricular compliance), but more often involve regulation of both phases of diastole. In asymptomatic patients with arterial hypertension, left ventricular relaxation is often prolonged, independently, at least in part, of cardiac loading conditions and left ventricular geometry, but this abnormality is associated with early signs of systolic dysfunction. Uncontrolled hypertension, diabetes, and obesity are most often associated with ischemic heart disease and impaired diastolic function. Reducing blood pressure with antihypertension therapy will reduce myocardial afterload, regress LVH, and improve systolic and diastolic function. In patients with symptoms of CHF with a normal ejection fraction, however, changes in therapy may be indicated. Greater emphasis should be placed on using medications that decrease myocardial load, but also reduce the effects of neurohormonal activation. (c)2001 by Le Jacq Communications, Inc.

Antihypertensive Agents↗
PubMed1994

Neuroendocrine activation in relation to left ventricular function in chronic severe congestive heart failure: a subgroup analysis from the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS).

Left ventricular (LV) function and plasma levels of cardiovascular hormones were examined in patients with severe chronic congestive heart failure (CHF), randomized to placebo or enalapril, in addition to conventional therapy. M-mode echocardiography and plasma hormone concentrations were available at baseline and after 6 weeks of treatment. There was a significant relationship between LV systolic function and levels of angiotensin-II and norepinephrine. Enalapril increased LV fractional shortening (FS%) (13.3 +/- 5.6 to 15.4 +/- 5.8, p < 0.05) and decreased the systolic time interval index (0.58 +/- 0.14 to 0.48 +/- 0.15, p < 0.05) concurrent with a significant decrease in angiotensin-converting enzyme activity and in aldosterone, angiotensin-II, and norepinephrine concentrations after 6 weeks. No changes were found in the placebo group. However, there was no direct relationship between the amount of change in neurohormones and improvement in LV function after 6 weeks. These findings indicate that in patients with severe chronic CHF, severe LV systolic dysfunction is associated with high plasma levels of angiotensin-II and norepinephrine, which can be favorably modified by enalapril. This may be of importance for prolonging life in severe heart failure. The lack of relationship between changes in individual hormones and systolic function suggests complex dynamic interaction. It is, therefore, not sufficient to predict changes in LV function by measuring changes in only one hormone.

Aldosterone↗
PubMed2000

Coronary reserve and arteriolosclerosis in hypertensive heart disease.

Hypertensive heart disease leads to left ventricular hypertrophy, structural and functional alterations of the myocardium, and to wall thickening and sclerosis of intramural coronary arteries and arterioles, called arteriolosclerosis, that increase myocardial stiffness and cause diastolic dysfunction right from the beginning. Especially, increased content of collagen in the periarteriolar region contributes to impaired coronary reserve that predisposes to myocardial ischemia even in the absence of coronary artery disease and may be an important factor for diastolic and finally systolic dysfunction. Antihypertensive therapy should additionally aim at inducing repair of myocardial and vascular structure.

Animals↗
PubMed2003

Long-term survival in patients hospitalized with congestive heart failure: relation to preserved and reduced left ventricular systolic function.

AIMS: The purpose of this study was to evaluate the influence of left ventricular systolic function on the survival in a large consecutive cohort of patients hospitalized with congestive heart failure and to determine how left ventricular systolic function interacts with co-morbid conditions in terms of prognosis. METHODS AND RESULTS: Analysis of survival data from 5491 patients admitted for new or worsening heart failure to 34 departments of cardiology or internal medicine in Denmark from 1993-1996 was carried out. A standardized echocardiogram was available for 95% of the patients, and left ventricular systolic function was estimated using wall motion index score. Follow-up time was 5-8 years. Patients with preserved systolic function were older, more frequently female, and had less evidence of ischemia than patients with systolic dysfunction. After 1 year, 24% of the patients had died. Low wall motion index was a potent independent predictor of death (risk ratio for one unit increase, 0.60 (0.56-0.64)), and was of greater prognostic significance in younger patients and patients with a history of myocardial ischemia. However, even in patients with preserved systolic function, mortality was high (1 year mortality, 19%). CONCLUSION: In hospitalized heart failure patients, particularly in younger patients with ischemic heart disease, mortality risk is inversely related to left ventricular systolic function.

Aged↗
PubMed1995

Left ventricular hypertrophy and diastolic dysfunction: their relation to coronary heart disease.

Diastolic dysfunction is an early sign in the temporal sequence of ischemic events in coronary heart disease. The ischemic cascade, beginning with an oxygen demand supply imbalance and metabolic alterations, identifies diastolic disorders of the left ventricle (LV) as an early phenomenon, sometimes before systolic dysfunction, electrocardiographic changes, or chest pain occur. Although the physiology of diastolic function is complex, the factors contributing to diastolic disturbances can be differentiated into intrinsic and extrinsic LV abnormalities. Intrinsic mechanisms include (a) impaired LV relaxation, (b) the complex of LV hypertrophy, and (c) increased LV asynchrony. Myocardial hypertrophy leads to an increase of the myocardial mass/volume ratio, and the degree of hypertrophy is the main determinant of chamber stiffness. The main, if not unique, determinant of myocardial diastolic tissue distensibility is the structure and concentration of the collagen. Consequently, tissue stiffness is increased in coronary disease by reparative interstitial fibrosis or scar following myocardial infarction. In myocardial hypertrophy the LV collagen concentration is elevated due to reactive fibrosis. An increase in regional asynchrony of LV contraction and relaxation is a result of regional ischemia as well as of LV hypertrophy and tissue fibrosis. Factors extrinsic to the LV causing diastolic disorders include (a) increased central blood volume, which will increase left ventricular pressure without altering the LV pressure-volume relation, and (b) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic LV pressure-volume relation. Improved insight into the mechanisms of LV relaxation and filling characteristics help in the treatment of LV diastolic dysfunction.

Coronary Disease↗
PubMed2006

Correlation and prognostic utility of B-type natriuretic peptide and its amino-terminal fragment in patients with chronic kidney disease.

This study compared the correlation and prognostic utility of B-type natriuretic peptide (BNP) and the N-terminal fragment of proBNP (NT-proBNP) in 171 outpatients with renal dysfunction. The NT-proBNP correlated well with BNP in all cases (r = 0.911; P pound .01), regardless of degree of renal impairment or type of left ventricular dysfunction. BNP and NT-proBNP concentrations (P < .005) and their ratios (P pound .01) increased as the glomerular filtration rate (GFR) declined, indicating a greater effect of GFR on NT-proBNP levels. Both natriuretic peptide levels were higher in patients with systolic dysfunction (P < .05) compared with patients with normal echocardiograms. In contrast, BNP and NT-proBNP levels were below the diagnostic cutoffs for congestive heart failure exacerbations in patients with normal heart function or diastolic dysfunction, with no statistical difference between these groups (P = .99). Both peptides are useful prognostic tools for predicting mortality and cardiac hospitalization in renal patients.

Aged↗