Impaired subendocardial perfusion in patients with metabolic syndrome

Background Metabolic Syndrome (MS) is associated to vascular damage, increased arterial stiffness, and impaired myocardial perfusion. Subendocardial viability ratio (SEVR) is a noninvasive estimation of myocardial workload, oxygen supply, and perfusion. The aim of the study was to describe the relation between arterial stiffness, SEVR, and cardio-metabolic risk factors. Methods A cohort of 55 patients, aged 59.9 ± 10.8 years, was studied; 28 subjects (50.9%) had metabolic syndrome. All patients underwent a clinical evaluation and blood venous sampling, to assess glico-lipid profile. Applanation tonometry was performed, to obtain pulse wave analysis and SEVR values. Results In the overall study population, SEVR showed negative associations with mean (r = −0.301; p = 0.026) and systolic (borderline relation, r = −0.257; p = 0.058) arterial pressure. Metabolic syndrome patients presented lower level of SEVR ( p = 0.012), even after adjusting for age, sex, and mean arterial pressure ( p = 0.040). Subdividing the study population by the number of metabolic syndrome components, SEVR significantly decreased as the number of Metabolic Syndrome components increased ( p for trend 0.005). In a logistic backward regression analysis, both metabolic syndrome and mean arterial pressure resulted significant predictors of SEVR, accounting for 18% of variance. Conclusion The reduced SEVR in metabolic syndrome patients could be an important pathophysiological determinant of the increased cardiovascular risk.

Disparate Information Provided by Pulse Wave Velocity versus Other Measures of Aortic Compliance in End-Stage Renal Disease

<b><i>Introduction:</i></b> Unfavorable changes in cardiac and arterial function are related to poor prognosis in chronic kidney disease (CKD). We compared hemodynamic profiles between subjects with end-stage renal disease and 2 control groups with corresponding pulse wave velocities (PWVs). <b><i>Methods:</i></b> Noninvasive hemodynamics were recorded during passive head-up tilt in CKD stage 5 patients (<i>n</i> = 35), patients with primary hypertension (<i>n</i> = 35, <i>n</i> = 30 with antihypertensive medications), and subjects without cardiovascular or renal diseases and cardiovascular medications (<i>n</i> = 70). The groups were selected to have corresponding age, sex, body mass index, and PWV. Hemodynamic data were captured using whole-body impedance cardiography and radial tonometric pulse wave analysis. <b><i>Results:</i></b> Supine blood pressure did not differ between the groups, but upright diastolic blood pressure was lower in CKD patients than in the 2 control groups (<i>p</i> ≤ 0.001 for both, RANOVA). Despite similar PWV, supine aortic pulse pressure was higher in CKD patients versus nonmedicated subjects (<i>p</i> = 0.029). Two additional measures indicated reduced aortic compliance in CKD patients versus both control groups: lower ratio of stroke index to aortic pulse pressure (<i>p</i> ≤ 0.023) and higher aortic characteristic impedance (<i>p</i> ≤ 0.003). The subendocardial viability ratio was lower in the CKD group than in both control groups (<i>p</i> ≤ 0.039). <b><i>Conclusion:</i></b> In the absence of differences in PWV, higher aortic pulse pressure and characteristic impedance, and lower ratio of stroke index to aortic pulse pressure, suggest reduced aortic compliance and impaired left ventricular function in CKD patients. A lower subendocardial viability ratio predisposes the CKD patients to impaired cardiac oxygen supply versus hypertensive patients and nonmedicated controls.

Six-Week Exercise Training With Dietary Restriction Improves Central Hemodynamics Associated With Altered Gut Microbiota in Adolescents With Obesity

PurposeObesity in children and in adolescents can lead to adult cardiovascular diseases, and the gut microbiota plays a crucial role in obesity pathophysiology. Exercise and diet interventions are typical approaches to improve physical condition and to alter the gut microbiota in individuals with obesity. However, whether central hemodynamic parameters including subendocardial viability ratio, the augmentation index standardized to a heart rate of 75/min (AIx75), resting heart rate, and blood pressure, correlate with gut microbiota changes associated with exercise and diet is unclear.MethodsAdolescents (n = 24, 12.88 ± 0.41 years) with obesity completed our 6-week program of endurance and strength exercises along with dietary restriction. Blood and fecal samples were collected, and physical parameters were measured before and 24 h after the last session of the intervention program. Pulse wave analysis using applanation tonometry provided the subendocardial viability ratio, a surrogate measure of microvascular myocardial perfusion, and AIx75, a measure of arterial stiffness and peripheral arteriolar resistance. Correlation analysis detected any associations of anthropometric or central hemodynamic parameters with gut microbiome composition.ResultsExercise and diet interventions significantly reduced body weight, body mass index, body fat, and waist-to-hip ratio, and lowered levels of fasting blood glucose, serum triglycerides, and high-density lipoprotein cholesterol. AIx75 and resting heart rate were also significantly reduced after the intervention without changes to systolic or diastolic blood pressure. The ratio of intestinal microbiota Firmicutes to Bacteroidetes displayed a marked increase after intervention. Interventional changes in gut microbiota members were significantly associated with anthropometric and metabolic parameters. Microbial changes were also significantly correlated with central hemodynamic parameters, including subendocardial viability ratio, AIx75, and resting heart rate.ConclusionExercise and diet interventions significantly improved measures of central hemodynamics, including subendocardial viability ratio, AIx75, and resting heart rate, which were correlated with altered gut microbiota in adolescents with obesity. Our findings shed light on the effects and mechanisms underlying exercise and diet interventions on obesity and suggest this approach for treating patients with both cardiovascular disease and obesity.

Insulin Increases The Central-To-Peripheral Arterial Stiffness Gradient in Response To Hyperglycemia in Healthy Humans: A Randomized Four-Way Crossover Study

Background: Increasing arterial stiffness is a physiological feature of vascular aging that is accelerated by conditions that enhance cardiovascular risk, including diabetes mellitus. Emerging evidence demonstrates that reversal of the normal central-to-peripheral arterial stiffness gradient predicts adverse cardiovascular consequences, including target organ damage. Preferential stiffening of central over peripheral arteries has been reported in type 2 diabetes, though mechanisms for this remain unclear.Methods: We tested the effect of acutely increasing plasma glucose, plasma insulin, or both on central arterial stiffness (carotid-femoral pulse wave velocity) and peripheral arterial stiffness (radial artery augmentation index) in a randomized, four-way, crossover study of 19 healthy young adults. We also measured myocardial oxygen supply-demand (subendocardial viability ratio) and hemodynamic function. Results: Carotid-femoral pulse wave velocity increased during hyperglycemic-hyperinsulinemia (+0.4 m/s; p=0.02) but not with euglycemia, hyperglycemia, or euglycemic-hyperinsulinemia. There were no significant changes in radial artery augmentation index within any protocol (all p>0.05), though this value trended lower with hyperglycemic-hyperinsulinemia (opposite of the observed effect on carotid-femoral pulse wave velocity). No changes were observed in subendocardial viability ratio within any protocol. Heart rate significantly increased only during hyperglycemic-hyperinsulinemia (+3.62 bpm; p=0.02). There was a significant inverse correlation between peripheral and arterial stiffness during hyperglycemic-hyperinsulinemia. Conclusions: We conclude that combined hyperglycemia and hyperinsulinemia acutely increases aortic stiffness, diminishes the normal central-to-peripheral arterial stiffness gradient, and increases heart rate in healthy humans. (ClinicalTrials.gov number NCT03520569; registered 9 May 2018).Clinical Trial Information: ClinicalTrials.gov identifier NCT03520569 (registered 9 May 2018).