Regional Myocardial Blood Flow and Glucose Utilization in Symptomatic Patients With Hypertrophic Cardiomyopathy

BackgroundPrevious studies suggested the presence of myocardial ischemia in symptomatic patients with hypertrophic cardiomyopathy. Positron emission tomography, a technique that can identify metabolic consequences of ischemia in coronary artery disease, permits the noninvasive measurements of regional myocardial blood flow and glucose metabolism. This new quantitative imaging approach should therefore be suitable for detecting a possible enhancement of glucose utilization in myocardium of patients with hypertrophic cardiomyopathy and thus may help to elucidate the pathomechanism of ischemia in this disease. Methods and ResultsIn 13 symptomatic patients with hypertrophic cardiomyopathy, myocardial blood flow and glucose utilization were measured with intravenous N-13-ammonia and F-18 deoxyglucose at rest and, in four patients, again during supine bicycle exercise. At rest, blood flow was significantly lower in hypertrophied than in normal myocardium (0.0$78.19 versus 0.99 $ 0.13 mL min'-1? g-1, P<0.025), whereas rates of glucose utilization were similar (0.88$031 versus 0.87$0.35, $um;mOl. min-1 g-1). With exercise, blood flow and glucose utilization failed to increase in hypertrophic and normal segments but became more heterogeneously distributed throughout the left ventricular myocardium. Blood flowmetabolism mismatches indicative of myocardial ischemia were noted in three patients at rest and in three of the four patients during exercise and were due to reduced flow in the presence of maintained glucose uptake. The discordance between flow and glucose metabolism in hypertrophied myocardium was significantly more prominent in younger than in older patients. ConclusionsNormal or even elevated rates of glucose utilization and the presence of diminished blood flow in hypertrophied relative to normal myocardium suggest the presence of myocardial ischemia in symptomatic hypertrophic cardiomyopathy. The age dependence of blood flow metabolism disparity suggests differences in the underlying pathophysiology or severity of disease.

[1]  Y. Kanno,et al.  Differences in myocardial fluoro-18 2-deoxyglucose uptake in young versus older patients with hypertrophic cardiomyopathy. , 1992, The American journal of cardiology.

[2]  E. Fisman,et al.  Sudden unexpected death in persons <40 years of age , 1991 .

[3]  A. Quyyumi,et al.  Myocardial Metabolic, Hemodynamic, and Electrocardiographic Significance of Reversible Thallium‐201 Abnormalities in Hypertrophic Cardiomyopathy , 1991, Circulation.

[4]  A. L'Abbate,et al.  Coronary vasodilation is impaired in both hypertrophied and nonhypertrophied myocardium of patients with hypertrophic cardiomyopathy: a study with nitrogen-13 ammonia and positron emission tomography. , 1991, Journal of the American College of Cardiology.

[5]  M. Phelps,et al.  A quantitative index of regional blood flow in canine myocardium derived noninvasively with N-13 ammonia and dynamic positron emission tomography. , 1991, Journal of the American College of Cardiology.

[6]  C. Nienaber,et al.  Syncope in hypertrophic cardiomyopathy: multivariate analysis of prognostic determinants. , 1990, Journal of the American College of Cardiology.

[7]  B. Maron,et al.  Relation between extent of left ventricular hypertrophy and diastolic filling abnormalities in hypertrophic cardiomyopathy. , 1990, Journal of the American College of Cardiology.

[8]  S. Gambhir Quantitation of the physical factors affecting the tracer kinetic modeling of cardiac positron emission tomography data , 1990 .

[9]  M. Phelps,et al.  PET detection of viable tissue in myocardial segments with persistent defects at T1-201 SPECT. , 1989, Radiology.

[10]  M. Phelps,et al.  Simple noninvasive quantification method for measuring myocardial glucose utilization in humans employing positron emission tomography and fluorine-18 deoxyglucose. , 1989, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[11]  M. Schwaiger,et al.  Sustained nonoxidative glucose utilization and depletion of glycogen in reperfused canine myocardium. , 1989, Journal of the American College of Cardiology.

[12]  M. Phelps,et al.  Regional myocardial blood flow and metabolism at rest in mildly symptomatic patients with hypertrophic cardiomyopathy. , 1989, Journal of the American College of Cardiology.

[13]  Michael E. Phelps,et al.  Semiautomatic Software For Quantitative Analysis Of Cardiac Positron Tomography Studies , 1988, Medical Imaging.

[14]  K. Kuck,et al.  Programmed electrical stimulation in hypertrophic cardiomyopathy. Results in patients with and without cardiac arrest or syncope. , 1988, European heart journal.

[15]  E. Hoffman,et al.  Validation of PET-acquired input functions for cardiac studies. , 1988, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[16]  S. Larson,et al.  Myocardial perfusion abnormalities in patients with hypertrophic cardiomyopathy: assessment with thallium-201 emission computed tomography. , 1987, Circulation.

[17]  C. Tracy,et al.  Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy. , 1987, Journal of the American College of Cardiology.

[18]  M. Matsuda,et al.  Quantitative analysis of narrowings of intramyocardial small arteries in normal hearts, hypertensive hearts, and hearts with hypertrophic cardiomyopathy. , 1987, Circulation.

[19]  W. Roberts,et al.  Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy. , 1986, Journal of the American College of Cardiology.

[20]  T. Spinks,et al.  Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina. , 1986, Circulation.

[21]  Michael E. Phelps,et al.  Dynamic, Gated and High Resolution Imaging with the ECAT III , 1986, IEEE Transactions on Nuclear Science.

[22]  C. Patlak,et al.  Graphical Evaluation of Blood-to-Brain Transfer Constants from Multiple-Time Uptake Data. Generalizations , 1985, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[23]  P Kligfield,et al.  Electrocardiographic detection of left ventricular hypertrophy: development and prospective validation of improved criteria. , 1985, Journal of the American College of Cardiology.

[24]  B. Maron,et al.  Diastolic abnormalities in patients with hypertrophic cardiomyopathy: relation to magnitude of left ventricular hypertrophy. , 1985, Circulation.

[25]  W. Williams,et al.  Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review. , 1985, Progress in cardiovascular diseases.

[26]  R. Bonow,et al.  Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures. , 1985, Circulation.

[27]  N. Tamaki,et al.  Recognition of regional hypertrophy in hypertrophic cardiomyopathy using thallium-201 emission-computed tomography: comparison with two-dimensional echocardiography. , 1984, The American journal of cardiology.

[28]  W. McKenna,et al.  Distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy: a two-dimensional echocardiographic study. , 1983, Journal of the American College of Cardiology.

[29]  M E Phelps,et al.  Positron tomography with deoxyglucose for estimating local myocardial glucose metabolism. , 1982, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[30]  M. Phelps,et al.  Glucose Metabolism during Ischemia Due to Excessive Oxygen Demand or Altered Coronary Flow in the Isolated Arterially Perfused Rabbit Septum , 1981, Circulation research.

[31]  D. Kuhl,et al.  N‐13 Ammonia as an Indicator of Myocardial Blood Flow , 1981, Circulation.

[32]  W. Mckenna,et al.  Prognosis in hypertrophic cardiomyopathy: role of age and clinical, electrocardiographic and hemodynamic features. , 1981, The American journal of cardiology.

[33]  D. Mathey,et al.  Myocardial thallium 201 imaging in hypertrophic obstructive cardiomyopathy. , 1981, European heart journal.

[34]  E. Braunwald,et al.  Improved diastolic function and systolic performance in hypertrophic cardiomyopathy after nifedipine. , 1980, The New England journal of medicine.

[35]  K. R. Anderson,et al.  Histopathological specificity of hypertrophic obstructive cardiomyopathy. Myocardial fibre disarray and myocardial fibrosis. , 1980, British heart journal.

[36]  W. Roberts,et al.  Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. , 1979, The American journal of cardiology.

[37]  A. DeMaria,et al.  Recommendations Regarding Quantitation in M-Mode Echocardiography: Results of a Survey of Echocardiographic Measurements , 1978, Circulation.

[38]  Opie Lh Effects of regional ischemia on metabolism of glucose and fatty acids. Relative rates of aerobic and anaerobic energy production during myocardial infarction and comparison with effects of anoxia. , 1976 .

[39]  J. Gaddum THE PHARMACOLOGICAL BASIS OF THERAPEUTICS , 1941, Nature.