Effects of propranolol on myocardial oxygen consumption, substrate extraction, and haemodynamics in hypertrophic obstructive cardiomyopathy.

Thompson, D S; Naqvi, N; Juul, S M; Swanton, R. H.; Coltart, D J; Jenkins, B S; Webb-Peploe, M M

doi:10.1136/hrt.44.5.488

Cited by 91 publications

(27 citation statements)

References 38 publications

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“…The present study demonstrates that MVO 2 in HCM patients is comparable to controls, in line with invasive investigations [21][22][23]. Similarly, previous non-invasive [ 11 C]acetate PET studies in HCM have demonstrated MVO 2 in HCM to be comparable to controls [24] or slightly decreased [2,25].…”

Section: Myocardial Oxygen Consumptionsupporting

confidence: 90%

“…However, when corrected for LVM, EW and PVA generated per gram of myocardium were significantly decreased in HCM, in line with other invasive [22] and non-invasive studies [2,24]. Although not reaching statistical significant, a trend towards an increased slope of the ESPVR was observed in the HCM group, consistent with an invasive study [26].…”

Section: Myocardial Oxygen Consumptionsupporting

confidence: 86%

“…Correspondingly, an early invasive study by Thompson and co-workers in 13 patients with obstructive HCM revealed an MEE of 21% [22]. Patients with LVH due to hypertension show similar pseudonormalization of MVO 2 , accompanied by decreased EW generation per gram of myocardium [27], suggesting that mechanoenergetic uncoupling is a distinctive feature in pathological hypertrophy [8,10].…”

Section: Myocardial Efficiencymentioning

confidence: 93%

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Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Timmer

Germans

Götte

et al. 2010

Eur J Nucl Med Mol Imaging

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Purpose Next to hypertrophy, hypertrophic cardiomyopathy (HCM) is characterized by alterations in myocardial energetics. A small number of studies have shown that myocardial external efficiency (MEE), defined by external work (EW) in relation to myocardial oxidative metabolism (MVO 2 ), is reduced. The present study was conducted to identify determinants of MEE in patients with HCM by use of dynamic positron emission tomography (PET) and cardiovascular magnetic resonance imaging (CMR). Methods Twenty patients with HCM (12 men, mean age: 55.2 ± 13.9 years) and 11 healthy controls (7 men, mean age: 48.1 ± 10 years) were studied with [ 11 C]acetate PET to assess MVO 2 . CMR was performed to determine left ventricular (LV) volumes and mass (LVM). Univariate and multivariate analyses were employed to determine independent predictors of myocardial efficiency.Results Between study groups, MVO 2 (controls: 0.12 ± 0.04 ml·min −1 ·g −1 , HCM: 0.13 ± 0.05 ml·min −1 ·g −1 , p = 0.64) and EW (controls: 9,139 ± 2,484 mmHg·ml, HCM: 9,368 ± 2,907 mmHg·ml, p = 0.83) were comparable, whereas LVM was significantly higher (controls: 99 ± 21 g, HCM: 200 ± 76 g, p < 0.001) and MEE was decreased in HCM patients (controls: 35 ± 8%, HCM: 21 ± 10%, p < 0.001). MEE was related to stroke volume (SV), LV outflow tract gradient, NH 2 -terminal pro-brain natriuretic peptide (NT-proBNP) and serum free fatty acid levels (all p < 0.05). Multivariate analysis revealed that SV (ß = 0.74, p < 0.001) and LVM (ß = −0.43, p = 0.013) were independently related to MEE. Conclusion HCM is characterized by unaltered MVO 2 , impaired EW generation per gram of myocardial tissue and subsequent deteriorated myocardial efficiency. Mechanical external efficiency could independently be predicted by SV and LVM.

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Section: Myocardial Oxygen Consumptionsupporting

confidence: 90%

Section: Myocardial Oxygen Consumptionsupporting

confidence: 86%

Section: Myocardial Efficiencymentioning

confidence: 93%

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Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Timmer

Germans

Götte

et al. 2010

Eur J Nucl Med Mol Imaging

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“…Thus, the verapamil dosage at the time of repeat study ranged from 240 to 480 mg/day (mean, 453), and this dosage was maintained for a mean of 6.7 days (range, 2-56) before the repeat study. The verapamil studies were performed [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] weeks (mean, 6±5) after the initial control studies.…”

Section: Study Protocolmentioning

confidence: 99%

Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy.

et al. 1989

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Recent studies indicate that reversible 201Tl perfusion defects, compatible with silent myocardial ischemia, commonly develop during exercise in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy (HCM). To determine whether this represents a dynamic process that may be modified favorably by medical therapy, we studied 29 asymptomatic or minimally symptomatic patients with HCM, aged 12-55 years (mean, 28), with exercise 201Tl emission computed tomography under control conditions and again after 1 week of oral verapamil (mean dosage, 453 mg/day). Treadmill time increased slightly during verapamil (21.0 +/- 3.6 to 21.9 +/- 2.7 minutes, p less than 0.005), but peak heart rate-blood pressure product was unchanged (26.3 +/- 6.0 X 10(3) compared with 25.0 +/- 6.4 X 10(3). Two midventricular short-axis images per study were divided into five regions each, and each of these 10 regions was then analyzed on a 0-2 scale by three observers blinded with regard to the patients' therapy. Average regional scores of 1.5 or less were considered to represent perfusion defects, and a change in regional score of 0.5 or more was considered to constitute a significant change. During control studies, 15 patients (52%) developed perfusion defects with exercise (average, 3.7 regions per patient). In 14 of these patients, all perfusion defects completely reversed after 3 hours of rest; one patient had fixed defects. After administration of verapamil, exercise perfusion scores improved in 10 of the 14 patients (71%) with reversible defects; there was overall improvement in 34 of 50 (68%) regions with initially reversible perfusion defects.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…mechanisms were reported for the exacerbated I/R injury of the hypertrophied hearts, including imbalance between myocardial oxygen supply and demand (1). This imbalance is caused by inadequate capillary density in relation to the increased myocardial mass and limitation of blood flow despite high oxygen demand of the myocardium (9,(33)(34)(35). Therefore, it could exacerbate the myocardial injury after ischemia (5,21,22).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Diazepam on the Function of Hypertrophied Rats’ Hearts in Ischemia-Reperfusion Conditions

Shackebaei¹,

Feizollahi²,

Hesari³

et al. 2016

Int Cardiovasc Res J

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A B S T R A C TBackground: Hypertrophied hearts are susceptible to ischemic injury. Besides, cardiac vulnerability could be changed in the presence of diazepam. Objectives: The current study aimed to investigate the effect of diazepam on hypertrophied rats' hearts in ischemia-reperfusion conditions. Materials and Methods: Male Wistar rats (body weight 210 -270 gr) were administered with isoproterenol (4 mg/kg body weight, intraperitoneally for 7 days) alone or along with diazepam (1 and 5 mg/kg body weight, intraperitoneally for 5 days). The control rats received normal saline intraperitoneally. The animal s' hearts were isolated according to langendorff setup and were passed through baseline, ischemia, and reperfusion stages. Then, cardiac mass index (ratio of heart weight to body weight) was measured. Cardiac functional parameters, including left ventricular developed pressure and rate pressure product, were also assessed at baseline and following ischemia. The data were analyzed using ANOVA and P < 0.05 was considered to be statistically significant. Results: Isoproterenol-induced cardiac hypertrophy was significantly reduced by both doses of diazepam compared to the group only treated with isoproterenol (P < 0.05) although it did not reach the control level. However, diazepam administration (1 and 5 mg/kg) did not change isoproterenol-induced exacerbated ischemia-reperfusion injury compared to the control group (P = 0.001 and P = 0.013, respectively). Conclusions: Diazepam relatively prevented the isoproterenol-induced cardiac hypertrophy in the animal model. This effect could be probably explained by the modification of oxidative stress and preservation of intracellular calcium concentration. Considering the common clinical usage of diazepam, as a peripheral benzodiazepine ligand, antihypertrophic effects of diazepam are recommended to be investigated in clinical trials.

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Effects of propranolol on myocardial oxygen consumption, substrate extraction, and haemodynamics in hypertrophic obstructive cardiomyopathy.

Cited by 91 publications

References 38 publications

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Determinants of myocardial energetics and efficiency in symptomatic hypertrophic cardiomyopathy

Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy.

The Effect of Diazepam on the Function of Hypertrophied Rats’ Hearts in Ischemia-Reperfusion Conditions

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