Sarcolemmal calcium transport in congestive heart failure due to myocardial infarction in rats

Because Na(+)-Ca2+ exchange and Ca2+ pump are thought to play a role in sarcolemmal Ca2+ movements, we examined the Na(+)-dependent Ca(2+)-uptake and ATP-dependent Ca(2+)-uptake activities in failing heart after myocardial infarction in rats. The left coronary artery was ligated, and the viable left ventricle was used 4, 8, and 16 wk later; sham-operated animals served as controls. Increased left ventricular diastolic pressure and decreased positive and negative change in pressure over time were observed in experimental animals at 4, 8, and 16 wk; these changes were associated with accumulation of fluid in the abdominal cavity. The sarcolemmal Na(+)-dependent Ca2+ uptake was depressed in 4-, 8-, and 16-wk experimental hearts. The decrease in sarcolemmal Na(+)-dependent Ca2+ uptake in failing hearts was seen when the activity was assayed either as a function of time or Ca2+ concentration; a depression of maximal velocity without any change in activity constant for Ca2+ was observed. No alteration in the Ca2+ pump (ATP-dependent Ca2+ accumulation and Ca(2+)-stimulated adenosinetriphosphatase) activities was evident in the 4-, 8-, and 16-wk experimental groups. These data suggest that changes in the Na(+)-dependent Ca2+ handling by the sarcolemmal membrane may be associated with contractile abnormalities in this model of congestive heart failure.

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Sarcolemmal Na(+)-K(+)-ATPase activity in congestive heart failure due to myocardial infarction

AJP Cell Physiology ◽

10.1152/ajpcell.1992.262.3.c664 ◽

1992 ◽

Vol 262 (3) ◽

pp. C664-C671 ◽

Cited By ~ 81

Author(s):

I. M. Dixon ◽

T. Hata ◽

N. S. Dhalla

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Congestive Heart Failure ◽

Atpase Activity ◽

Abdominal Cavity ◽

Clinical Signs ◽

Left Ventricular ◽

Ph Optimum ◽

Hemodynamic Assessment ◽

Cardiac Pump Function

Because the Na+ pump is considered to modulate the contractile force development by the cardiac muscle and depressed cardiac pump function is the hallmark of congestive heart failure, we characterized the sarcolemmal Na(+)-K(+)-ATPase activity in failing rat hearts after myocardial infarction. For this purpose, the left ventricular coronary artery was ligated, and hearts were examined 4, 8, and 16 wk later; sham-operated animals served as controls. Hemodynamic assessment revealed the presence of abnormal cardiac function at 4, 8, and 16 wk. Although accumulation of ascites in the abdominal cavity was present in experimental animals at 4 wk, other clinical signs of congestive heart failure in experimental rats including lung congestion and cardiac dilatation were evident 8 and 16 wk after induction of myocardial infarction. The depression in Na(+)-K(+)-ATPase activity in purified sarcolemmal membrane from the uninfarcted experimental left ventricle at 8 wk was associated with depressed Vmax without any changes in the affinities for Mg-ATP, Na+, and K+ or the pH optimum for the enzyme. The Kd values of both the high- and low-affinity binding sites for [3H]ouabain, which is believed to interact with Na(+)-K(+)-ATPase, were increased; however, no change in the density of either class of ouabain binding site was evident. The depression of Na(+)-K(+)-ATPase activity in failing hearts at 16 wk of myocardial infarction was not different from that observed at 8 wk but the enzyme activity was not altered at 4 wk of coronary occlusion. These data support the view that depression of Na(+)-K(+)-ATPase activity may serve as an adaptive mechanism during the development of congestive heart failure.

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Influence of Age on the Prognostic Importance of Left Ventricular Dysfunction and Congestive Heart Failure on Long-Term Survival After Acute Myocardial Infarction

The American Journal of Cardiology ◽

10.1016/s0002-9149(96)00250-0 ◽

1996 ◽

Vol 78 (2) ◽

pp. 158-162 ◽

Cited By ~ 4

Author(s):

L Køber, MD

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Acute Myocardial Infarction ◽

Congestive Heart Failure ◽

Left Ventricular Dysfunction ◽

Ventricular Dysfunction ◽

Left Ventricular ◽

Term Survival ◽

Prognostic Importance

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Congestive Heart Failure in Copper-Deficient Mice

Experimental Biology and Medicine ◽

10.1177/15353702-0322807-06 ◽

2003 ◽

Vol 228 (7) ◽

pp. 811-817 ◽

Cited By ~ 44

Author(s):

Laila Elsherif ◽

Raymond V. Ortines ◽

Jack T. Saari ◽

Y. James Kang

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Left Ventricle ◽

Diastolic Pressure ◽

Systolic Pressure ◽

Pressure Rise ◽

Experimental Models ◽

Left Ventricular ◽

Mouse Heart ◽

Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

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Myocardial Infarction in Neonates: A Diagnostic and Therapeutic Challenge

Case Reports in Pediatrics ◽

10.1155/2019/7203407 ◽

2019 ◽

Vol 2019 ◽

pp. 1-5

Author(s):

Manuel Rodríguez Martínez ◽

Eladio Ruiz González ◽

Anna Parra-Llorca ◽

Máximo Vento Torres ◽

Marta Aguar Carrascosa

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Acute Myocardial Infarction ◽

Congestive Heart Failure ◽

Left Atrial ◽

Left Atrial Appendage ◽

Ventricular Dysfunction ◽

Left Ventricular ◽

Cardiac Enzymes ◽

Term Baby

Neonatal acute myocardial infarction is an uncommon entity. We describe the case of a 4-day-old term baby who presented with respiratory distress and distal acrocyanosis. The chest radiograph demonstrated cardiomegaly without pleural effusion, and examination revealed hepatomegaly. An electrocardiogram revealed QS pattern in leads I, aVL, and V6, suggestive of ischemia. Cardiac enzymes were elevated, and echocardiogram revealed moderate left ventricular dysfunction with a thrombus at the level of the left atrial appendage. The patient required hemodynamic stabilization, vasodilatation to avoid congestive heart failure, and anticoagulation with heparin and aspirin. In the context of this unusual diagnosis, we reviewed our experience over the last 17 years as well as the existing literature on neonatal myocardial infarction.

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Expectoration of bronchial casts in association with Ramipril treatment

Cardiology in the Young ◽

10.1017/s1047951119002294 ◽

2019 ◽

Vol 29 (12) ◽

pp. 1565-1566

Author(s):

Kim Sarah Plümacher ◽

Thomas Paul ◽

Matthias Sigler

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Diastolic Pressure ◽

Acute Myocarditis ◽

Parvovirus B19 ◽

Virus Genome ◽

Left Ventricular ◽

Myocardial Biopsy ◽

Bronchial Cast ◽

Bronchial Casts

AbstractWe report of a 26-year-old female patient who was referred to our centre with congestive heart failure (CHF). Acute myocarditis with a high Parvovirus B19 virus load was diagnosed by myocardial biopsy. CHF improved after start of ramipril 5 mg/d, metoprolol, diuretics, immunoglobins, and a 24-hour infusion of levosimendan. Soon after initiation of medical therapy, the patient started to expectorate bronchial casts with varying frequencies (three times per week to five times daily). Thorough pneumological workup, including histology of the casts, microbiology, and a CT scan of the lungs, did not reveal any cause for bronchial cast formation. Inhalative corticoids were started without any benefit. Two years later, cardiac catheterisation demonstrated normalised left ventricular function. LV end-diastolic pressure, however, was still elevated at 14 mmHg. Endomyocardial biopsies at this time were negative for virus genome. Finally, we changed afterload reduction therapy from ramipril to candesartan. Within 24 hours, expectoration of bronchial casts terminated. Four weeks later, re-exposition to ramipril prompted immediate re-appearance of cast formation, which again stopped with switching back to candesartan. Finally, we were to prove that treatment with ramipril resulted in bronchial cast formation in this patient.

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Vascular β-adrenergic receptor system is dysfunctional after myocardial infarction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.3.h1129 ◽

2001 ◽

Vol 280 (3) ◽

pp. H1129-H1135 ◽

Cited By ~ 8

Author(s):

Mohamed A. Gaballa ◽

Andrea Eckhart ◽

Walter J. Koch ◽

Steven Goldman

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Carotid Artery ◽

Membrane Protein ◽

Adrenergic Receptor ◽

Vascular Reactivity ◽

Diastolic Pressure ◽

Systolic Pressure ◽

Left Ventricular ◽

Receptor System

We identified abnormalities in the vascular β-adrenergic receptor (β-AR) signaling pathway in heart failure after myocardial infarction (MI). To examine these abnormalities, we measured β-AR-mediated hemodynamics, vascular reactivity, and the vascular β-AR molecular signaling components in rats with heart failure after MI. Six weeks after MI, these rats had an increased left ventricular (LV) end-diastolic pressure, decreased LV systolic pressure, and decreased rate of LV pressure change (dP/d t). LV dP/d t responses to isoproterenol were shifted downward, although the responses for systemic vascular resistance were shifted upward in heart failure rats ( P < 0.05). Isoproterenol- and IBMX-induced vasorelaxations were blunted in heart failure rats ( P< 0.05) with no change in the forskolin-mediated vasorelaxation. These changes were associated with the following alterations in β-AR signaling ( P < 0.05): decreases in β-AR density (aorta: 58.7 ± 6.0 vs. 35.7 ± 1.9 fmol/mg membrane protein; carotid: 29.6 ± 5.6 vs. 18.0 ± 3.9 fmol/mg membrane protein, n = 5), increases in G protein-coupled receptor kinase activity levels (relative phosphorimage counts of 191 ± 39 vs. 259 ± 26 in the aorta and 115 ± 30 vs. 202 ± 7 in the carotid artery, n = 5), and decreases in cGMP and cAMP in the carotid artery (0.85 ± 0.10 vs. 0.31 ± 0.06 pmol/mg protein and 2.3 ± 0.3 vs. 1.2 ± 0.1 pmol/mg protein, n = 5) with no change in Gαs or Gαi in the aorta. Thus in heart failure there are abnormalities in the vascular β-AR system that are similar to those seen in the myocardium. This suggests a common neurohormonal mechanism and raises the possibility that treatment in heart failure focused on the myocardium may also affect the vasculature.

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