Among patients with TIMI flow grade 3, the extent of microvascular damage, detected and quantitated by MCE, is the most powerful independent predictor of LV remodeling after STEMI as compared with persistent ST-segment elevation and myocardial blush grade.

AimsFew data are available on the extent and prognostic value of reverse left ventricular remodelling (r-LVR) after ST-elevation acute myocardial infarction (STEMI). We sought to evaluate incidence, major determinants, and long-term clinical significance of r-LVR in a group of STEMI patients treated with primary percutaneous coronary intervention (PPCI). In particular, the role of preserved microvascular flow within the infarct zone in inducing r-LVR has been investigated.Methods and resultsSerial echocardiograms (2DE) and myocardial contrast study were obtained within 24 h of coronary recanalization (T1) and at pre-discharge (T2) in 110 reperfused STEMI patients. Follow-up 2DE was scheduled after 6 months (T3). Two-year clinical follow-up was obtained. Reverse remodelling was defined as a reduction >10% in LV end-systolic volume (LVESV) at 6 months follow-up. r-LVR occurred in 39% of study population. At multivariable analysis, independent predictors of r-LVR were an effective microvascular reflow within the infarct zone, the in-hospital improvement of myocardial perfusion, an initial large LVESV, and a short time to reperfusion. Cox analysis identified r-LVR as the only independent predictor of 2-year event-free survival. Combined events rate was significantly higher among patients without compared to those with r-LVR (log-rank test P < 0.05).Conclusionr-LVR frequently occurs in STEMI patients treated with PPCI and it is an important predictor of favourable long-term outcome. A preserved microvascular perfusion within the infarct zone is the major determinant of r-LVR.

Metabolic syndrome (MS) is a multifactorial disease that can affect clinical outcomes in patients treated by Cardiac Resynchronization Therapy with a defibrillator (CRT-d).Ninety-one patients received a CRT-d. According to clinical diagnosis, the study population was divided into 46 MS (cases) versus 45 no MS (controls) patients. These patients were followed by clinical, instrumental assessment, and device telemetric interrogations at follow-up. The design of the study was to evaluate the functionality of the CRT-d leads, the arrhythmic events, the CRT-d response, and the clinical outcomes at follow-up.At follow-up, there was a statistical significant difference, comparing MS versus no MS patients regarding the sensing, pacing, and impedance thresholds of the right atrium, right ventricle, and left ventricle leads. There was a statistically significant difference in the percentage of CRT-d responders comparing MS (n = 16, 51%) versus no MS (n = 40, 77%) patients (P = 0.017). MS may be predictive for hospitalization for heart failure worsening (hazard ratio 0.327, 95% confidence interval 0.096-0.943, P = 0.044) in CRT-d patients.MS is a complex multifactorial disease that may affect the functionality of CRT-d leads, the CRT-d response, and clinical outcomes in failing heart patients. These parameters may be detectable by follow-up monitoring.Abbreviations: AF = atrial fibrillation, BMI = body mass index, CRP = C reactive protein, CRT-d = cardiac resynchronization therapy with a defibrillator, HF = heart failure, ICD = implantable cardioverter defibrillators, LV = left ventricle, LVEF = left ventricle ejection fraction, MS = metabolic syndrome, ms = milli second, mV = milli Volt, NYHA = New York Heart Association, RV = right ventricle, VF = ventricular fibrillation, VT = ventricular tachycardia.

Liver cirrhosis is associated with enlarged right cardiac chambers. Diastolic dysfunction and mild pulmonary hypertension are evident in cirrhotic patients with ascites. These changes do not depend on variations in the left ventricular geometry.

Our study demonstrates that nonalcoholic cirrhotic patients, without cardiovascular pathologies, show transient modifications in cardiac dimension and function for 3-6 months after TIPS caused by the increased volume load shunted to the heart.