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Gaps in evidence for risk stratification for sudden cardiac death in hypertrophic cardiomyopathy. circulation
No full textSudden cardiac death (SCD) is the most dramatic and catastrophic complication of hypertrophic cardiomyopathy (HCM),1 with an annual rate of >1%.1 The identification of those patients most likely to benefit from prophylacticimplantable cardioverter defibrillators remains challenging in children and adults. The positive predictive value for appropriate discharges is low (≈20%), and the complication rates in this younger, active population is substantial, including lead problems, infections, inappropriate discharges, and psychological issue
Combined checkpoint inhibitor-associated myocarditis and pulmonary vasculitis mimicking acute pulmonary embolism
No full textMyocardial pre-synaptic sympathetic function correlates with glucose uptake in the failing human heart
No full textPURPOSE:
We have previously shown that the myocardium of patients with heart failure (HF) is insulin resistant. Chronic beta-adrenergic stimulation has been implicated in insulin resistance in cultured cardiomyocytes in vitro, where sustained noradrenaline stimulation inhibited insulin-modulated glucose uptake. As the failing heart is characterized by increased sympathetic drive, we hypothesized that there is a correlation between pre-synaptic sympathetic function and insulin sensitivity in the myocardium of patients with HF.
METHODS:
Eight patients (aged 67 +/- 7 years) with coronary artery disease and left ventricular dysfunction (ejection fraction 44 +/- 10%) underwent function and viability assessment with cardiovascular magnetic resonance. Myocardial glucose utilization (MGU) was measured using positron emission tomography (PET) with (18)F-fluorodeoxyglucose (FDG). Pre-synaptic noradrenaline re-uptake was measured by calculating [(11)C]meta-hydroxy-ephedrine (HED) volume of distribution (V (d)) with PET. Two groups of healthy volunteers served as controls for the FDG (n = 8, aged 52 +/- 4 years, p < 0.01 vs patients) and HED (n = 8, aged 40 +/- 6 years, p < 0.01 vs patients) data.
RESULTS:
MGU in patients was reduced in both normal remote (0.44 +/- 0.14 micromol.min(-1).g(-1)) and dysfunctional (0.49 +/- 0.14 micromol.min(-1).g(-1)) segments compared with controls (0.61 +/- 0.7 micromol.min(-1).g(-1); p < 0.001 vs both). HED V (d) was reduced in dysfunctional segments of patients (38.9 +/- 21.2 ml.g(-1)) compared with normal segments (52.2 +/- 19.6 ml.g(-1)) and compared with controls (62.7 +/- 11.3 ml.g(-1)). In patients, regional MGU was correlated with HED V (d).
CONCLUSION:
The results of this study provide novel evidence of a correlation between cardiac sympathetic function and insulin sensitivity, which may represent one of the mechanisms contributing to insulin resistance in failing human hearts
Coronary microvascular dysfunction in hypertensive patients with left ventricular hypertrophy can be reversed by treatment with a fixed combination of perindropril and indapamide
No full textBackground: Patients (pts) with arterial hypertension (Ht) and left ventricular hypertrophy (LVH) are at high risk of developing cardiac events. They often complain of angina and have ST segment depression during stress suggesting myocardial ischemia despite angiographically normal coronary arteries in most cases. This is due to coronary microvascular dysfunction caused by remodelling of intramural coronary arterioles which can be assessed non-invasively by measuring myocardial blood flow (MBF) using positron emission tomography (PET). Aim of this study was to ascertain whether pharmacologic treatment with a fixed combination of perindopril+indapamide can improve coronary microvascular dysfunction in pts with Ht and LVH.
Methods: Fifteen pts (mean age 60±6 years, 5 females) with arterial Ht (≥140/90 and <180/110 mmHg) complicated by LVH, with no evidence of other organ damage or concomitant disease and in therapy wash-out (1 to 4 weeks depending on preceding treatment) were studied. At baseline LV mass (LVM) was measured by cardiovascular magnetic resonance (CMR) and absolute resting and hyperemic (dipyridamole 0.56 mg/kg) MBF was measured by PET with nitrogen-13 labelled ammonia. CMR and PET scans were repeated after 6 months of therapy. The initial dosage of the combination was 2/0.625 mg (perindopril and indapamide, respectively) which was titrated, if needed, up to 8/2.5 mg during follow up.
Results: SBP decreased from 160±11 (mean±SD) to 140±15 mmHg (p<0.01), DBP from 97±6 to 83±7 mmHg (p<0.0001) and LVM from 159±39 to 146±34 g (p<0.05). Resting MBF increased from 0.67±0.13 to 0.91±0.38 (M6) ml/min/g (p<0.001) and maximum MBF during dipyridamole from 1.45±0.31 to 2.03±1.14 ml/min/g (p=0.06).
Conclusions: Six month treatment with perindopril+indapamide in pts with Ht and LVH causes a significant decrease in SBP, DBP and LVM which is accompanied by an increase in resting and hyperemic MBF. This suggests that coronary microvascular dysfunction can be reversed by treatment with these drugs and might contribute to the prevention of ischemic heart disease in these pts
Independent association of type 2 diabetes and coronary artery disease with myocardial insulin resistance
No full textReduced glucose transporter GLUT4 in skeletal muscle predicts insulin resistance in non-diabetic chronic heart failure patients independently of body composition.
No full textPredictors of mortality in myocardial infarction and nonobstructed coronary arteries. a systematic review and meta-regression
Full text linkBACKGROUND: The long-term mortality of patients with myocardial infarction and non-obstructed coronary arteries (MINOCA) remains poorly defined. This study aimed to determine long-term mortality of patients with MINOCA and identify potential prognostic determinants of long-term outcome. METHODS: We searched Pubmed, Embase and Cochrane databases and reviewed cited references up to December 31, 2018 to identify studies with > 6 months follow-up data. RESULTS: We selected 44 studies including 36,932 patients (20,052 women and 16,880 men). During a median follow-up of 25 months (interquartile range: 23-39 months), 1,409 patients had died (3.8%). Overall, annual mortality rate was 2.0% (95% CI: 1.5% to 2.4%) with significant heterogeneity (I2=80%, P<0.001). Meta-analysis of the 26 studies comparing patients with MINOCA with those with myocardial infarction and obstructive coronary artery disease showed that annual rates of long-term total mortality were 2.2% (95% CI: 1.7-2.7%) and 5.0% (95% CI: 4.1-5,9%) respectively, with a significant difference between the two groups (Relative Risk: 0.60, 95% CI: 0.46-0.78, p<0.001). Meta-regression analysis demonstrated that normal ejection fraction (p=<0.0001) and normal coronary arteries at angiography (p=0.004) were inversely related to long-term mortality whilst use of beta-blockers during follow-up (p=0.010) and ST depression on the admission electrocardiogram (p=0.016) were directly related with worse outcome. CONCLUSIONS: The long-term mortality after MINOCA is lower than that in patients with myocardial infarction and obstructive coronary artery disease, but it is not trivial. Reduced ejection fraction, non-obstructive coronary artery disease, use of beta-blockers during follow up and ST depression on the admission electrocardiogram are significant predictors of long-term prognosis. (PROSPERO registration number CRD42019117042)
Increased myocardial uptake of lipids and impaired utilization of lactate and pyruvate in patients with mild to moderate high blood pressure
No full textMismatch between insulin-mediated glucose uptake and blood flow in the heart of patients with Type II diabetes
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