Cardiac syndrome X versus metabolic syndrome X

Cheng, Tsung O.

doi:10.1016/j.ijcard.2006.06.062

Cited by 16 publications

(15 citation statements)

References 16 publications

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“…Reaven coined the term "syndrome X" to describe the clustering abnormalities associated with insulin resistance but since another syndrome X had been documented in cardiology, 2 the term insulin resistance syndrome became more frequently used to describe what should have been legitimately called the Reaven syndrome. It is also relevant to mention that as Reaven found insulin resistant individuals who were not obese, he did not include obesity as a feature of the insulin resistance syndrome.…”

Section: The Pioneermentioning

confidence: 99%

Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk

Després¹,

Lemieux²,

Bergeron³

et al. 2008

ATVB

1,346

940

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There is currently substantial confusion between the conceptual definition of the metabolic syndrome and the clinical screening parameters and cut-off values proposed by various organizations (NCEP-ATP III, IDF, WHO, etc) to identify individuals with the metabolic syndrome. Although it is clear that in vivo insulin resistance is a key abnormality associated with an atherogenic, prothrombotic, and inflammatory profile which has been named by some the “metabolic syndrome” or by others “syndrome X” or “insulin resistance syndrome”, it is more and more recognized that the most prevalent form of this constellation of metabolic abnormalities linked to insulin resistance is found in patients with abdominal obesity, especially with an excess of intra-abdominal or visceral adipose tissue. We have previously proposed that visceral obesity may represent a clinical intermediate phenotype reflecting the relative inability of subcutaneous adipose tissue to act as a protective metabolic sink for the clearance and storage of the extra energy derived from dietary triglycerides, leading to ectopic fat deposition in visceral adipose depots, skeletal muscle, liver, heart, etc. Thus, visceral obesity may partly be a marker of a dysmetabolic state and partly a cause of the metabolic syndrome. Although waist circumference is a better marker of abdominal fat accumulation than the body mass index, an elevated waistline alone is not sufficient to diagnose visceral obesity and we have proposed that an elevated fasting triglyceride concentration could represent, when waist circumference is increased, a simple clinical marker of excess visceral/ectopic fat. Finally, a clinical diagnosis of visceral obesity, insulin resistance, or of the metabolic syndrome is not sufficient to assess global risk of cardiovascular disease. To achieve this goal, physicians should first pay attention to the classical risk factors while also considering the additional risk resulting from the presence of abdominal obesity and the metabolic syndrome, such global risk being defined as cardiometabolic risk.

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Section: The Pioneermentioning

confidence: 99%

Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk

Després¹,

Lemieux²,

Bergeron³

et al. 2008

ATVB

1,346

940

View full text Add to dashboard Cite

show abstract

“…Clinical Implications. Detection of coronary microvascular disease in the MetS is essential for appropriate treatment, especially since microvascular angina is common in this patient population (52)(53)(54). Clinically, adenosine stress testing is used to examine for myocardial perfusion defects at the microvascular level.…”

Section: Discussionmentioning

confidence: 99%

Altered Mechanism of Adenosine-Induced Coronary Arteriolar Dilation in Early-Stage Metabolic Syndrome

Bender

Tune

Borbouse

et al. 2009

Exp Biol Med (Maywood)

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Onset of the combined metabolic syndrome (MetS) is a complex progressive process involving numerous cardiovascular risk factors. Although patients with established MetS exhibit reduced coronary flow reserve and individual components of the MetS reduce microvascular vasodilation, little is known concerning the impact of early-stage MetS on the mechanisms of coronary flow control. Therefore, we tested the hypothesis that coronary arteriolar dilation to adenosine is attenuated in early-stage MetS by reduced A2 receptor function and diminished K+ channel involvement. Pigs were fed control or high-fat/cholesterol diet for 9 weeks to induce early-stage MetS. Coronary atheroma was determined in vivo with intravascular ultrasound. In vivo coronary dilation was determined by intracoronary adenosine infusion. Further, apical coronary arterioles were isolated, cannulated and pressurized to 60 cmH2O for in vitro pharmacologic assessment of adenosine dilation. Coronary atheroma was not different between groups, indicating early-stage MetS. Coronary arteriolar dilation to adenosine (in vivo) and 2-chloroadenosine (2-CAD; in vitro) was similar between groups. In control arterioles, 2-CAD-mediated dilation was reduced only by selective A2A receptor inhibition, whereas only dual A2A/2B inhibition reduced this response in MetS arterioles. Arteriolar A2B, but not A2A, receptor protein expression was reduced by MetS. Blockade of voltage-dependent K+ (Kv) channels reduced arteriolar sensitivity to 2-CAD in both groups, whereas ATP-sensitive K+ (KATP) channel inhibition reduced sensitivity only in control arterioles. Our data indicate that the mechanisms mediating coronary arteriolar dilation to adenosine are altered in early-stage MetS prior to overt decrements in coronary vasodilator reserve.

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“…Investigators have demonstrated that patients with MetSx are susceptible to endothelial dysfunction [6,7]. This is supported by the observed higher prevalence of MetSx among patients with chest pain and demonstrable myocardial ischemia in the setting of angiographically normal coronary arteries [8], suggesting a link between MetSx and coronary syndrome X [9,10]. Patients with slow filling of distal coronary arteries in the absence of significant epicardial coronary artery disease, a sign of microcirculatory impairment, are more likely to have MetSx [11,12], implying that MetSx has detrimental effects at the microcirculatory level.…”

Section: Introductionmentioning

confidence: 94%

Likelihood of obstructive coronary disease in metabolic syndrome patients with abnormal stress echocardiography

Badarin

From

McCully

et al. 2011

International Journal of Cardiology

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Cardiac syndrome X versus metabolic syndrome X

Cited by 16 publications

References 16 publications

Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk

Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk

Altered Mechanism of Adenosine-Induced Coronary Arteriolar Dilation in Early-Stage Metabolic Syndrome

Likelihood of obstructive coronary disease in metabolic syndrome patients with abnormal stress echocardiography

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