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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Transl Res. 2017 Jan 9;183:57–70. doi: 10.1016/j.trsl.2017.01.001

Figure.

Figure

Schematic diagram of the pathologic features, adverse molecular and systemic changes, and cardiovascular consequences of the metabolic syndrome. Clustering of causally inter-related risk factors including abdominal obesity, impaired glucose tolerance, hypertriglyceridemia, decreased HDL cholesterol, and/or hypertension is associated activation of the sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS), and increased levels of pro-inflammatory adipokines and cytokines. These phenotypic changes subsequently contribute to increases in heart rate, circulating blood volume, cardiac output, vascular resistance, and changes in myocardial metabolism. The consequences of these changes include microvascular dysfunction, cardiac contractile dysfunction (augmented end-diastolic volume and systemic pressure development observed in left ventricular pressure-volume relationship (data from Sassoon et al.(52)), atherosclerotic disease (L = lumen; M = media; image of human coronary artery from Noblet et al.(170)), vascular calcification (arrow points to calcification; image provided by Dr. Michael Sturek with permission), concentric cardiac hypertrophy, myocardial infarction, and heart failure.