Ultrasonographic assessment of coronary flow reserve and abdominal fat in obesity

Kondô, Isao; Mizushige, Katsufumi; Hirao, Kenichi; Nozaki, Shiro; Tsuji, Takao; Masugata, Hisashi; Kohno, Masakazu; Matsuo, Hirohíde

doi:10.1016/s0301-5629(01)00427-6

Cited by 28 publications

(26 citation statements)

References 22 publications

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“…It is important to recognize that the 21 Ϯ 1% stenosis in metabolic syndrome swine did not limit flow during hyperemia, since the peak hyperemic response (i.e., the minimum vascular resistance) and volume of repayment were not different between lean and metabolic syndrome swine (Table 2). Our finding is consistent with earlier studies demonstrating decreases in coronary flow reserve (8,10,31,33,46) and impaired ischemic peripheral (forearm, calf) vasodilation (1,11,29) in obese human patients. In addition, these data extend our earlier observation that metabolic syndrome significantly impairs metabolic control of coronary blood flow at rest and during exercise-induced increases in MVO 2 (47,50).…”

Section: Effect Of Metabolic Syndrome On Ischemic Coronary Vasodilationsupporting

confidence: 94%

“…Recent evidence also indicates that peripheral (forearm, calf) vasodilation in response to ischemia is significantly impaired in obese and type 2 diabetic human patients (1,11,29). Although coronary flow reserve is reduced by obesity and metabolic syndrome (8,10,31,33,46), no study has examined the effects of metabolic syndrome on ischemic coronary vasodilation. Based on recent data indicating that metabolic syndrome impairs the function of vascular smooth muscle K ϩ channels (3,4,7,13,25,40), we propose that metabolic syndrome attenuates coronary reactive hyperemia via alterations in the contribution of specific K ϩ channels to ischemic vasodilation.…”

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confidence: 97%

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Metabolic syndrome reduces the contribution of K⁺ channels to ischemic coronary vasodilation

Borbouse

Dick

Payne

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K(+) channels to coronary reactive hyperemia. Ca(2+)-activated (BK(Ca)), voltage-activated (K(V)), and ATP-dependent (K(ATP)) K(+) channels were investigated. Studies were conducted in anesthetized miniature Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BK(Ca) (penitrem A; 10 microg/kg iv), K(V) (4-aminopyridine; 0.3 mg/kg iv) and K(ATP) (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced approximately 30% compared with lean swine. Inhibition of BK(Ca) channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of K(V) channels significantly reduced the repayment of flow debt ( approximately 25%) in both lean and metabolic syndrome swine. Additional blockade of K(ATP) channels further diminished ( approximately 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K(+) channels to reactive hyperemia.

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Section: Effect Of Metabolic Syndrome On Ischemic Coronary Vasodilationsupporting

confidence: 94%

mentioning

confidence: 97%

Metabolic syndrome reduces the contribution of K⁺ channels to ischemic coronary vasodilation

Borbouse

Dick

Payne

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…Currently, ultrasonography is not a widely used method for assessing body fat, either in HIV-infected patients or in the general population. However, this method has already been validated in several studies, and correlates well with measurements obtained using computerized tomography (CT), offering several relative advantages over the latter [6,7,[29][30][31][32] . Martinez et al [33] has also used ultrasound to evaluate body fat distribution in HIV-infected patients.…”

Section: Discussionmentioning

confidence: 99%

Ultrasonographic Measurement of Intra-Abdominal Fat Thickness in HIV-Infected Patients Treated or Not with Antiretroviral Drugs and Its Correlation to Lipid and Glycemic Profiles

Mm¹,

Ar²,

Mg³

et al. 2007

Ann Nutr Metab

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Aims: To compare the intra-abdominal fat thickness measured by ultrasound between HIV-infected patients treated or not with antiretroviral drugs and to correlate these visceral adiposity measurements to other parameters of cardiovascular risks. Methods: In a transversal observational study, 160 HIV-infected patients were recruited and divided in two groups, i.e., 123 antiretroviral (ARV)-treated and 37 ARV-naïve patients. These patients were submitted to anthropometric determinations, laboratorial analysis, ultrasonographic measurements of subcutaneous and intra- abdominal fat thickness and to tetrapolar bioelectrical impedance analysis in order to measure the body composition. Results: In the patients treated with highly active antiretroviral therapy (HAART) the intra-abdominal fat pad was significantly thicker than that of the untreated group (69 ± 21 mm, n = 123 vs. 60 ± 18 mm, n = 37; p = 0.03 Student’s t test). The intra-abdominal fat thickness correlated significantly with plasma triglyceride, total cholesterol, fasting glucose, glucose measurements 2 h after dextrose load, fasting insulin, HOMA-IR index, systolic and diastolic blood pressures, weight, BMI, WHR and caliper-measured total fat percentage. Conclusion: The results showed that antiretroviral therapy is associated with increased ultrasonographic measurements of visceral adiposity. Our data demonstrated a strong correlation between intra-abdominal fat thickness and independent risk factors of cardiovascular disease: atherogenic lipid profile and insulin resistance.

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“…From a clinical point of view, it is important to note that maximal density of macrophages/mm 2 in atherosclerotic lesions is associated with visceral obesity (30), reduced coronary flow reserve related to body fat distribution and insulin resistance (31), and the MetS associated with lipid-rich plaque (32). In a systematic review and meta-analysis of longitudinal studies (33), it has been reported that individuals with the MetS are at increased risk of a cardiovascular events and death (relative risk 1.78).…”

Section: Coronary Artery Diseasementioning

confidence: 99%

Targeting abdominal obesity in cardiology: Can we be effective?

Poirier

2008

Canadian Journal of Cardiology

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Ultrasonographic assessment of coronary flow reserve and abdominal fat in obesity

Cited by 28 publications

References 22 publications

Metabolic syndrome reduces the contribution of K⁺ channels to ischemic coronary vasodilation

Metabolic syndrome reduces the contribution of K⁺ channels to ischemic coronary vasodilation

Ultrasonographic Measurement of Intra-Abdominal Fat Thickness in HIV-Infected Patients Treated or Not with Antiretroviral Drugs and Its Correlation to Lipid and Glycemic Profiles

Targeting abdominal obesity in cardiology: Can we be effective?

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Ultrasonographic assessment of coronary flow reserve and abdominal fat in obesity

Cited by 28 publications

References 22 publications

Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation

Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation

Ultrasonographic Measurement of Intra-Abdominal Fat Thickness in HIV-Infected Patients Treated or Not with Antiretroviral Drugs and Its Correlation to Lipid and Glycemic Profiles

Targeting abdominal obesity in cardiology: Can we be effective?

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Metabolic syndrome reduces the contribution of K⁺ channels to ischemic coronary vasodilation

Metabolic syndrome reduces the contribution of K⁺ channels to ischemic coronary vasodilation