Myocardial metabolic studies in prolapsing mitral leaflet syndrome.

Natarajan, Gangaiah; Nakhjavan, Fred K.; Kahn, D; Yazdanfar, Shahriar; Sahibzada, Waheed A.; Khawaja, Farhan J.; Goldberg, Harry

doi:10.1161/01.cir.52.6.1105

Cited by 35 publications

(9 citation statements)

References 13 publications

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“…Lactate extraction of less than 10% despite no net lactate production has been considered abnormal, for example, in subjects with normal coronary angiograms and chest pain'5 and patients with mitral valve prolapse. 16 Using isolated heart preparations, Williamson and Krebs`7 and Randle and associates'8 found that myocardial carbohydrate metabolism is dependent on the circulating concentration of ketone bodies and free fatty acids. Their isolated heart experiments have shown that myocardial lactate extraction can be completely inhibited in the presence of high levels of ketones and free fatty acids at a time when the heart is not hypoxic.…”

mentioning

confidence: 99%

Myocardial lactate extraction: multi-determined metabolic function.

Gertz¹,

Wisneski²,

Neese³

et al. 1980

Circulation

119

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Myocardial lactate production indicates anaerobic metabolism resulting from hypoxia or anoxia. Clinically, myocardial lactate extraction of less than 10% has also been used as an indicator of ischemia. Sixteen healthy young male volunteers underwent coronary sinus and aterial catheterization. A coronary sinus pacing catheter was used to obtain blood samples and increase the heart rate to twice the resting rate. Hemodynamic measurements and blood samples for lactate, free fatty acids and glucose were obtained at rest and during pacing. Seven of 16 sujects (44%) had lactate extraction of less than 10% at rest and/or at miximal pacing. No subject produced lactate. There was no correlation between myocardial lactate extraction and arterial glucose. However, lactate extraction correlated inversely with the arterial levels of free fatty acids (r = 0.67; p less than 0.01). In addition, a positive correlation was present between lactate extraction and the arterial lactate level (r = 0.78; p less than 0.01). In conclusion, myocardial lactate extraction is dependent on multiple metabolic parameters and any absolute value short of production cannot be considered abnormal.

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mentioning

confidence: 99%

Myocardial lactate extraction: multi-determined metabolic function.

Gertz¹,

Wisneski²,

Neese³

et al. 1980

Circulation

119

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“…30,31 Within the current study group, patients with severe regurgitation (nϭ11, 1.29Ϯ0.3, PϽ.02), dyspneic subjects (nϭ10, 1.21Ϯ0.24, PϽ.003), and those on therapy for heart failure (nϭ13, 1.29Ϯ0.29, PϽ.01) had significantly lower ratios compared with control subjects (nϭ13, 1.61Ϯ0.3). However, the control ratio was not significantly different from the ratio in patients classified echocardiographically with mild or moderate disease, among patients without dyspnea, or in those who did not require treatment for heart failure.…”

Section: Pcr/atp: Mr Compared With Control Subjectsmentioning

confidence: 80%

“…33,37,38 Altered biochemistry is reported by other investigators who studied patients with mitral valve prolapse. The arterial and coronary sinus blood lactate levels were increased 30 in a group with mitral valve prolapse, and right ventricular endomyocardial biopsies 31 demonstrated evidence of mitochondrial degeneration. However, some investigators (eg, Chidsey et al 39 ) have reported normal high-energy phosphorus metabolism in the papillary muscle of patients with MR compared with myocardial tissue from congenital heart disease patients.…”

Section: Figurementioning

confidence: 96%

Mitral Regurgitation

et al. 1998

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Background-A number of phosphorus ( 31 P) magnetic resonance spectroscopy (MRS) studies link alterations of high-energy phosphate metabolism in valvular disease and cardiomyopathy to the clinical severity of heart failure. However, correlations between MRS and indexes of ventricular dysfunction are inconclusive to date. We examined whether changes in 31 P MRS are associated with the impaired contractility, which predisposes to chronic congestive heart failure in patients with mitral regurgitation. Methods and Results-Thirteen normal control subjects and 22 patients with echocardiographically characterized chronic mitral regurgitation were studied by 31 P MRS. The apical phosphocreatine-to-ATP ratio (PCr/ATP) was lower in severe disease (PϽ.02) and those on therapy (nϭ13, 1.29Ϯ0.29, PϽ.01) in contrast to control subjects (nϭ13, 1.61Ϯ0.3). Compared to those with mild mitral regurgitation, patients with more severe incompetence had lower mean myocardial PCr/ATP ratios (mild, nϭ6,

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“…It could be suggested that the metabolic or haemodynamic abnormalities, which have been shown to occur in these syndromes, result in myocardial cell injury (Samet, 1973;Natarajan et al, 1975). These damaged cells may then be capable of taking up pyrophosphate.…”

Section: Discussionmentioning

confidence: 99%