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

Abstract

To assess regional coronary reserve in hypertrophic cardiomyopathy, regional myocardial blood flow was measured in 23 patients with hypertrophic cardiomyopathy and 12 control subjects by means of nitrogen-13 ammonia and dynamic positron emission tomography. In patients with hypertrophic cardiomyopathy at baseline study, regional myocardial blood flow was 1.14 +/- 0.43 ml/min per g in the hypertrophied (20 +/- 3 mm) interventricular septum and 0.90 +/- 0.35 ml/min per g (p less than 0.05 versus septal flow) in the nonhypertrophied (10 +/- 2 mm) left ventricular free wall. These were not statistically different from the corresponding values in control subjects (1.04 +/- 0.25 and 0.91 +/- 0.21 ml/min per g, respectively, p = NS). After pharmacologically induced coronary vasodilation (dipyridamole, 0.56 mg/kg intravenously over 4 min), regional myocardial blood flow in patients with hypertrophic cardiomyopathy increased significantly less than in control subjects both in the septum (1.63 +/- 0.58 versus 2.99 +/- 1.06 ml/min per g, p less than 0.001) and in the free wall (1.47 +/- 0.58 versus 2.44 +/- 0.82 ml/min per g, p less than 0.001). In addition, patients with hypertrophic cardiomyopathy who had a history of chest pain had more pronounced impairment of coronary vasodilator reserve than did those without a history of chest pain. After dipyridamole, coronary resistance in the septum decreased by 38% in patients without a history of chest pain, but decreased by only 14% in those with such a history (p less than 0.05). Coronary resistance in the free wall decreased by 45% in patients without and by 27% in those with a history of chest pain (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

“…Microvascular dysfunction results in a blunted perfusion reserve [31,32] and subsequent myocardial ischaemia during stress [33], even in the non-hypertrophied LV free wall [32]. Therefore, in analogy to ischaemic heart disease due to CAD, repetitive stunning of the myocardium in HCM might contribute to deteriorating efficiency.…”

Relationship between atrial fibrillation and blunted hyperemic myocardial blood flow in patients with hypertrophic cardiomyopathy

“…MBF was calculated from the dynamic data by fitting the arterial input function and tissue time-activity curves to a compartmental model for N-13 ammonia and the average hMBF for the entire LV was obtained. 11 We did not measure baseline MBF in order to minimize patient exposure, taking into account that previous studies demonstrate that this parameter is not significantly different between HCM patients and healthy controls 4 and that hMBF is superior to coronary flow reserve in predicting LV remodeling and outcome in HCM patients. 8,9 All studies were analyzed by expert observers, completely unaware of the patient clinical and echocardiographic data.…”

“…Then, dipyridamole was administered intravenously (0.56 mg/kg of body weight/ 4 minutes). 4 After 3 minutes of dipyridamole infusion, a bolus of 370 MBq of nitrogen-13 ammonia (N-13 ammonia) diluted in 10 mL saline solution was injected intravenously over a period of 15 to 20 seconds. A dynamic scan was acquired for the duration of 4 minutes, followed by a prolonged static acquisition of 15 minutes.…”

“…4,10 Briefly, patients were positioned on the PET scanner and a transmission scan was recorded. Then, dipyridamole was administered intravenously (0.56 mg/kg of body weight/ 4 minutes).…”

“…2,3 Coronary microvascular dysfunction (CMD), documented by positron emission tomography (PET) as a blunted response of myocardial blood flow to pharmacologically induced hyperemia (hMBF), is also a wellknown feature of HCM. 4,5 CMD has been identified as a powerful predictor of adverse outcome due to heart failure progression and death in HCM patients. [6][7][8][9] To date, it is unknown whether AF and CMD are associated, and whether the clinical consequences of CMD may be partly mediated by increased susceptibility to arrhythmia.…”