Is myocardial Na+/Ca2+ exchanger transcription a marker for different stages of myocardial dysfunction? Quantitative polymerase chain reaction of the messenger RNA in endomyocardial biopsies of patients with heart failure

Piper, Cornelia; Bilger, Johannes; Henrichs, Eva-Maria; Schultheiss, Heinz‐Peter; Horstkotte, Dieter; Doerner, Andrea

doi:10.1016/s0735-1097(00)00703-8

Cited by 16 publications

(16 citation statements)

References 37 publications

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“…Na + -Ca 2+ exchanger is important to maintain Ca 2+ homeostasis in the heart. It has been reported that the expression of this gene is elevated in the end stage of heart failure [30,31]. Our data from 16 weeks heart failure model are consistent with these previous observations.…”

Section: Discussionsupporting

confidence: 93%

Differential gene expression in infarct scar and viable myocardium from rat heart following coronary ligation

Chapman

Dixon

et al. 2004

J Cellular Molecular Medi

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Post‐myocardial infarction (MI) remodeling of cardiac myocytes and the myocardial interstitium results in alteration of gross ventricular geometry and ventricular dysfunction. To investigate the mechanisms of the remodeling process of the heart after large MI, the expression of various genes in viable left ventricle and infarct scar tissue were examined at 16 weeks post‐MI. Steady‐state expression of Na+‐K+ATPase α‐1 and −2, phospholamban (PLB), α‐myosin heavy chain (α‐MHC), ryanodine receptor (Rya) and Ca2+ ATPase (Serca2) mRNAs were decreased in the infarct scar vs noninfarcted sham‐operated controls (P < 0.05). On the other hand, Giα2 and β‐MHC mRNAs were upregulated (P < 0.05, respectively) in the infarct scar whereas Na+‐K+ ATPase‐β, Na+‐Ca2+ exchanger and Gs mRNAs were not altered vs control values. In viable left ventricle, the a‐1 subunit of Na+‐K+ATPase, α‐3, β‐isoforms, Rya, β‐MHC, Giα2, Gs and Na+‐Ca2+ exchanger were significantly elevated while expression of the a‐2 subunit of Na+‐K+ ATPase, PLB and Serca2 were significantly decreased compared to controls. Expression of CK2α mRNA was elevated in noninfarcted heart (145 ± 15%) and diminished in the infarct scar (66 ± 13%) vs controls. Expression of β‐MHC mRNA was elevated in both viable and infarct scar tissues of experimental hearts (140 ± 31% and 183 ± 30% vs. controls, respectively). These results suggest that cardiac genes in the infarcted tissue and viable left ventricle following MI are differentially regulated.

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Section: Discussionsupporting

confidence: 93%

Differential gene expression in infarct scar and viable myocardium from rat heart following coronary ligation

Chapman

Dixon

et al. 2004

J Cellular Molecular Medi

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“…We have now shown that a reduction in adrenergic myocardial contractile reserve appears to be associated with down-regulation not only of beta 1 -AR mRNA but also of SERCA2a and phospholamban mRNAs, even in asymptomatic or mildly symptomatic patients with DCM. On the other hand, we did not detect changes in the abundance of ryanodine receptor-2, calsequestrin, or Na ϩ / Ca 2ϩ exchanger mRNA in patients with a reduced adrenergic myocardial contractile reserve, which may be considered consistent with previous findings (21)(22)(23).…”

Section: Dobutamine Stress Test In Dcm Patientssupporting

confidence: 92%

Dobutamine Stress Testing as a Diagnostic Tool for Evaluation of Myocardial Contractile Reserve in Asymptomatic or Mildly Symptomatic Patients With Dilated Cardiomyopathy

Kobayashi

Izawa

Cheng

et al. 2008

JACC: Cardiovascular Imaging

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“…Studies in humans with heart failure have focused on examining changes in expression levels of proteins or genes involved in calcium signaling or measuring calcium concentrations and SR Ca 2ϩ uptake in cardiomyocytes isolated from failing hearts of transplant recipients at the time of surgery. [93][94][95] Such analyses remain to be conducted in patients with diabetic cardiomyopathy. However, a recent study described depressed myofilament function as a result of decreased Ca 2ϩ sensitivity in skinned fibers obtained from diabetic patients at the time of coronary artery bypass surgery.…”

Section: Impaired Calcium Homeostasismentioning

confidence: 99%

Diabetic Cardiomyopathy Revisited

2007

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Abstract-Diabetes mellitus increases the risk of heart failure independently of underlying coronary artery disease, and many believe that diabetes leads to cardiomyopathy. The underlying pathogenesis is partially understood. Several factors may contribute to the development of cardiac dysfunction in the absence of coronary artery disease in diabetes mellitus. This review discusses the latest findings in diabetic humans and in animal models and reviews emerging new mechanisms that may be involved in the development and progression of cardiac dysfunction in diabetes. (Circulation. 2007;115:3213-3223.)Key Words: diabetes mellitus Ⅲ fatty acids Ⅲ heart failure Ⅲ metabolism Ⅲ obesity T he prevalence of diabetes mellitus is growing rapidly. It is estimated that globally the number of adults affected with diabetes will increase from 135 million in 1995 to 300 million by 2025. 1 Patients with diabetes mellitus are at increased risk for cardiovascular diseases. Thus, cardiovascular complications are the leading cause of diabetes-related morbidity and mortality. 2 Diabetes mellitus is responsible for diverse cardiovascular complications such as increased atherosclerosis in large arteries (carotids, aorta, and femoral arteries) and increased coronary atherosclerosis, which increases the risk for myocardial infarction, stroke, and limb loss. Microangiopathy contributes to retinopathy and renal failure and may contribute to cardiac pathology as well. 3,4 Diabetes mellitus also can affect cardiac structure and function in the absence of changes in blood pressure and coronary artery disease, a condition called diabetic cardiomyopathy. This term was introduced 30 years ago by Rubler et al, 5 who described 4 diabetic patients with congestive heart failure and normal coronary arteries. Since then, diabetic cardiomyopathy has been defined as ventricular dysfunction that occurs independently of coronary artery disease and hypertension. In addition, diabetic cardiomyopathy may be characterized by diastolic dysfunction, which becomes more apparent in the presence of hypertension or myocardial ischemia (discussed in detail in the next section). Human StudiesMany epidemiological and clinical studies have suggested the existence of a diabetic cardiomyopathy in humans. 2,6 -9 Diabetes mellitus is a well-recognized risk factor for developing heart failure. Indeed, the Framingham Heart Study showed that the frequency of heart failure is twice in diabetic men and five times in diabetic women compared with age-matched control subjects. 10 This increased incidence of heart failure in diabetic patients persisted despite correction for age, hypertension, obesity, hypercholesterolemia, and coronary artery disease. Studies using independent population databases have provided similar results, revealing increased heart failure rates in subjects with diabetes mellitus in cross-sectional analyses and increased risk for developing heart failure in prospective analyses, even after correction for confounding variables. [11][12][13] Echocardiographic c...

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Is myocardial Na+/Ca2+ exchanger transcription a marker for different stages of myocardial dysfunction? Quantitative polymerase chain reaction of the messenger RNA in endomyocardial biopsies of patients with heart failure

Abstract: The upregulation in EXCH transcription either occurs very late in human heart failure or is a phenomenon of heart transplantation in end-stage HF. Consequently, myocardial EXCH transcription cannot be used as a marker for early myocardial decompensation.

Cited by 16 publications

References 37 publications

Differential gene expression in infarct scar and viable myocardium from rat heart following coronary ligation

Differential gene expression in infarct scar and viable myocardium from rat heart following coronary ligation

Dobutamine Stress Testing as a Diagnostic Tool for Evaluation of Myocardial Contractile Reserve in Asymptomatic or Mildly Symptomatic Patients With Dilated Cardiomyopathy

Diabetic Cardiomyopathy Revisited

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