We investigated whether left ventricular hypertrophy in elite cyclists is associated with functional changes or abnormal energy metabolism. Left ventricular hypertrophy is a powerful risk factor for sudden cardiac death with different prognostic significance among the various geometric forms. Cyclists may have a combination of mixed eccentric and concentric hypertrophy. Magnetic resonance imaging was used to define left ventricular mass, geometry and function. Thirteen highly trained male cyclists and 12 healthy controls were investigated. Proton-decoupled phosphorus-31 cardiac spectroscopy was performed to assess parameters of myocardial high-energy phosphate metabolism. Left ventricular mass and end-diastolic volumes normalized for body surface area were significantly higher in cyclists (124.1 +/- 9.4 g.m-2 and 106.2 +/- 11.4 ml.m-2, respectively) than in controls (85.9 +/- 9.3 g.m-2 and 79.1 +/- 11.6 ml.m-2, respectively), (both P < 0.0001). The left ventricular mass to end-diastolic volume ratio, as a parameter of left ventricular geometry, was not significantly increased in cyclists compared to controls. Resting left ventricular ejection fraction, cardiac index, and systolic wall stress in cyclists did not differ significantly from those of controls. The phosphocreatine to adenosine triphosphate ratio was not significantly different between cyclists and controls (2.2 +/- 0.34 vs 2.2 +/- 0.17, ns). Cyclists show prominent left ventricular hypertrophy with normal geometry. The finding that the hypertrophic hearts of the cyclists had normal left ventricular function and a normal phosphocreatine to adenosine triphosphate ratio suggests that sport-induced left ventricular hypertrophy is a physiological adaptation rather than a pathophysiological response.

We conclude that the ASE two-dimensional echocardiographic approach, when using magnetic resonance imaging as a reference standard, was the most accurate estimator of left ventricular mass and volumes in both controls and athletes.

Nisoldipine is a calcium antagonist with potent coronary vasodilating effects in patients with chronic stable angina pectoris. In an initial study we showed that intravenous nisoldipine, given 24-72 hours after uncomplicated myocardial infarction, was a safe and feasible intervention that had beneficial effects on global and regional myocardial function. We subsequently studied the acute effects of nisoldipine in six patients within 24 hours (mean 14 +/- 4 hours) after the onset of myocardial infarction. Nisoldipine was administered as a 4.5 micrograms/kg intravenous bolus over 3 minutes, followed by intravenous infusion of 0.2 microgram/kg over 60 minutes. Radionuclide angiography, cardiac output, and intraarterial blood pressure measurements were performed before and during nisoldipine. Left ventricular ejection fraction increased from 48.3 +/- 10.3% to 55.3 +/- 11.8% (p = 0.034) during nisoldipine infusion. Regional wall motion score changed during nisoldipine infusion from 3.3 +/- 2.5 to 1.8 +/- 2.6 (p = 0.027). Cardiac output increased from 5.5 +/- 1.0 to 7.3 +/- 1.3 l/min (p = 0.0001). Heart rate increased from 78 +/- 12 to 88 +/- 11 min-1 (p = 0.004). Mean arterial blood pressure decreased from 92 +/- 20 to 79 +/- 13 mmHg (p = 0.038). The rate-pressure product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine improves global and regional left ventricular function in patients with acute myocardial infarction within the first 24 hours.

Nisoldipine is a calcium antagonist with potent coronary vasodilating effects in patients with chronic stable angina pectoris. We studied the acute effects of nisoldipine in six patients within 24 h (mean 14 +/- 4 h) after the onset of myocardial infarction. Nisoldipine was administered as a 4.5 micrograms kg-1 intravenous bolus over 3 min followed by intravenous infusion of 0.2 microgram kg-1 min-1 during 60 min. Radionuclide angiography, cardiac output and intra-arterial blood pressure measurements were performed before and during nisoldipine. Left ventricular ejection fraction increased from 48.3 +/- 10.3% to 55.3 +/- 11.8% (P = 0.034) during nisoldipine infusion. Regional wall motion score changed during nisoldipine infusion from 3.3 +/- 2.5 to 1.8 +/- 2.6 (P = 0.027). Cardiac output increased from 5.5 +/- 1.0 to 7.3 +/- 1.3 l min-1 (P = 0.0001). Heart rate increased from 78 +/- 12 to 88 +/- 11 beats.min-1 (P = 0.004). Mean arterial blood pressure decreased from 91.7 +/- 20.2 to 78.7 +/- 13.1 mmHg (P = 0.038). The rate-pressure product did not change significantly during nisoldipine infusion. It is concluded that nisoldipine improves global and regional left ventricular function in patients with acute myocardial infarction within the first 24 h. Our findings suggest that this effect is achieved without increasing myocardial oxygen demand.

Funding Acknowledgements Type of funding sources: None. Introduction Patients (pts) with acute heart failure (AHF) are a heterogeneous population. The etiology of the heart disfunction may play a role in prognosis. Risk stratification at admission may help predict in-hospital complications and needs. Objective To explore predictors of in-hospital mortality (IHM), post discharge early mortality [1-month mortality (1mM)] and late mortality [1-year mortality (1yM)] and early and late readmission, respectively 1-month readmission (1mRA) and 1-year readmission (1yRA), in our center population, using real-life data. Methods Based on a single-center retrospective study, data collected from patients (pts) admitted in the Cardiology department with AHF between 2010 and 2017. Pts without data on previous cardiovascular history or uncompleted clinical data were excluded. The pts were divided in 3 groups: ischemic etiology (IE), valvular etiology (VE) and other etiologies (OE), which included hypertensive and idiopathic cardiomyopathies). Statistical analysis used non-parametric tests and Kaplan-Meyer survival analysis. Results We included 300 pts admitted with AHF. Mean age was 67.4 ± 12.6 years old and 72.7% were male. 37.7% had previous history of revascularization procedures, 66.9% had hypertension, 41% were diabetic and 38% had dyslipidaemia. The heart failure was of IE in 45%, VE in 22.7% and of OE in 32.3% of the cases. There were no significant differences between groups regarding body mass index, Killip-Kimball class, systolic blood pressure at admission, blood tests aspects at admission (namely, creatinine, sodium or urea), inotropes’ usage or need of non-invasive or invasive ventilation. However, IE group had higher percentage of males comparing to VE e OE (83.0% vs 55.9% vs 70.1%, respectively, p &lt; 0.001), higher rates of prior revascularization procedures (68.9%, vs 19.1%, vs 7.2%, p &lt; 0.001) and higher rates of traditional cardiovascular risk factors, namely hypertension (74.1% vs 55.9% vs 57.7%, p = 0.014), diabetes mellitus (48.1% vs 27.9% vs 27.8%, p = 0.002) and dyslipidaemia (48.9% vs 30.9% vs 40.2%, p = 0.022). OE group was younger compared to IE and VE (63.9 ± 13.5 vs 68.9 ± 11.1 vs 69.5 ± 13.0 years old, respectively, p = 0.003). VE group had less left ventricle disfunction comparing to IE and VE groups (left ventricle ejection fraction 40.8 ± 14.1 vs 32.2 ± 9.8 vs 31.6 ± 12.8%, respectively, p &lt; 0.001). The groups showed no significant differences regarding IHM (IE 5.2% vs VE 8.8% vs OE 2.1%, p = 0.146), 1mRA (IE 8.1&, VE 7.4%, OE 3.1%, p = 0.276) or 1yRA (IE 55.6%, VE 54.4%, OE 47.4%, p = 0.449). However, VE group had higher rates of 1mM (VE 13.2% vs IE 8.9% vs OE 3.1%, p = 0.05) and 1yM compared to IE and OE (33.8% vs 30.4% vs 17.5%, respectively, p = 0.34). These aspects are represented in Kaplan Meier survival curves. Conclusion In our population, the etiology of heart failure was predictor of early and late post-discharge mortality but not readmission.