Pericardial effusion unrelated to surgery is a predictor of mortality in heart transplant patients.

BACKGROUND: Hemodynamically irrelevant pericardial effusion (PeEf) is a predictor of adverse outcome in heart failure patients. The clinical relevance of a PeEf unrelated to surgery in heart transplant patients remains unknown. This study assesses the prognostic value of PeEf occurring later than 1 year after transplantation. METHODS: All patients undergoing heart transplantation in Zurich between 1989 and 2012 were screened. Cox proportional hazard models were used to analyze mortality (primary) and hospitalization (secondary endpoint). PeEf time points were compared to baseline for rejection, immunosuppressants, tumors, inflam-mation, heart failure, kidney function, hemodynamic, and echocardiographic parameters. RESULTS: Of 152 patients (mean age 48.3 ± 11.9), 25 developed PeEf. Median follow-up period was 11.9 (IQR 5.8-17) years. The number of deaths was 6 in the PeEf group and 46 in the non-PeEf group. The occurrence of PeEf was associated with a 2.5-fold increased risk of death (HR 2.49, 95% CI 1.02-6.13, p = 0.046) and hospitalization (HR 2.53, 95% CI 1.57-4.1, p = 0.0002). CONCLUSIONS: This study reveals that the finding of hemodynamically irrelevant PeEf in heart trans-plant patients is a predictor of adverse outcome, suggesting that a careful clinical assessment is war-ranted in heart transplant patients exhibiting small PeEf.

Coronary microvasculopathy in heart transplantation: Consequences and therapeutic implications.

Despite the progress made in the prevention and treatment of rejection of the transplanted heart, cardiac allograft vasculopathy (CAV) remains the main cause of death in late survival transplanted patients. CAV consists of a progressive diffuse intimal hyperplasia and the proliferation of vascular smooth muscle cells, ending in wall thickening of epicardial vessels, intramyocardial arteries (50-20 µm), arterioles (20-10 µm), and capillaries (< 10 µm). The etiology of CAV remains unclear; both immunologic and non-immunologic mechanisms contribute to endothelial damage with a sustained inflammatory response. The immunological factors involved are Human Leukocyte Antigen compatibility between donor and recipient, alloreactive T cells and the humoral immune system. The non-immunological factors are older donor age, ischemia-reperfusion time, hyperlipidemia and CMV infections. Diagnostic techniques that are able to assess microvascular function are lacking. Intravascular ultrasound and fractional flow reserve, when performed during coronary angiography, are able to detect epicardial coronary artery disease but are not sensitive enough to assess microvascular changes. Some authors have proposed an index of microcirculatory resistance during maximal hyperemia, which is calculated by dividing pressure by flow (distal pressure multiplied by the hyperemic mean transit time). Non-invasive methods to assess coronary physiology are stress echocardiography, coronary flow reserve by transthoracic Doppler echocardiography, single photon emission computed tomography, and perfusion cardiac magnetic resonance. In this review, we intend to analyze the mechanisms, consequences and therapeutic implications of microvascular dysfunction, including an extended citation of relevant literature data.

Different prognostic value of functional right ventricular parameters in arrhythmogenic right ventricular cardiomyopathy/dysplasia.

BACKGROUND: The value of standard 2-dimensional transthoracic echocardiographic parameters for risk stratification in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is controversial. METHODS AND RESULTS: We investigated the impact of RV fractional area change (FAC) and tricuspid annulus plane systolic excursion (TAPSE) for the prediction of major adverse cardiovascular events (MACE) defined as the occurrence of cardiac death, heart transplantation, survived sudden cardiac death, ventricular fibrillation, sustained ventricular tachycardia, or arrhythmogenic syncope. Among 70 patients who fulfilled the 2010 ARVC/D Revised Task Force Criteria and underwent baseline transthoracic echocardiography, 37 (53%) patients experienced MACE during a median follow-up period of 5.3 (interquartile range, 1.8-9.8) years. Average values for FAC, TAPSE, and TAPSE indexed to body surface area (BSA) decreased over time (P=0.03 for FAC, P=0.03 for TAPSE, and P=0.01 for TAPSE/BSA, each versus baseline). In contrast, median RV end-diastolic area increased (P=0.001 versus baseline). Based on the results of Kaplan-Meier estimates, the time between baseline transthoracic echocardiography and experiencing MACE was significantly shorter for patients with FAC <23% (P<0.001), TAPSE <17 mm (P=0.02), or right atrial short axis/BSA ≥25 mm/m(2) (P=0.04) at baseline. A reduced FAC constituted the strongest predictor of MACE (hazard ratio, 1.08 per 1% decrease; 95% confidence interval, 1.04-1.12; P<0.001) on bivariable analysis. CONCLUSIONS: This long-term observational study indicates that TAPSE and dilation of right-sided cardiac chambers are associated with an increased risk for MACE in patients with ARVC/D with advanced disease and a high risk for adverse events. However, FAC is the strongest echocardiographic predictor of adverse outcome in these patients. Our data advocate a role for transthoracic echocardiography in risk stratification in patients with ARVC/D, although our results may not be generalizable to lower-risk ARVC/D cohorts.

Impact of three-dimensional imaging and pressure recovery on echocardiographic evaluation of severe aortic stenosis: a pilot study.

AIMS: In patients with aortic stenosis (AS), echocardiographic grading of stenosis severity is important, in particular for transcatheter aortic valve implantation (TAVI). Three-dimensional (3D) echocardiography and correction for pressure recovery (PR) by energy loss index (ELI) may improve aortic valve area (AVA) calculation. METHODS AND RESULTS: Thirty-nine patients with severe AS evaluated for TAVI were included. Left ventricular outflow tract (LVOT) and ascending aorta (AA) cross-sectional area were determined in transthoracic two-dimensional echocardiography (2DTTE), 2D transesophageal echocardiography (TEE), 3DTEE, and multislice computed tomography (MSCT). AVA was calculated by the continuity equation and corrected for PR. ELI was determined as [(AVA × AA)/(AA - AVA)]/body surface area. LVOT area was 2.41 ± 0.17 cm(2) calculated using 2DTTE, 2.82 ± 0.16 cm(2) calculated using 2DTEE, 3.96 ± 0.14 cm(2) planimetered in 3DTEE, and 4.47 ± 0.18 cm(2) planimetered in MSCT (P < 0.001). AA area was 4.62 ± 0.23 cm(2) calculated using 2DTTE, 4.64 ± 0.23 cm(2) calculated using 2DTEE, 5.35 ± 0.25 cm(2) planimetered in 3DTEE, and 6.56 ± 0.31 cm(2) planimetered in MSCT (P < 0.001). Indexed aortic valve area (AVAI) calculated by 2DTTE and 2DTEE was smaller (0.27 ± 0.02 cm(2) /m(2) and 0.32 ± 0.02 cm(2) /m(2) ) compared to 3DTEE (0.45 ± 0.02 cm(2) /m(2) ; P < 0.001). When AVAI determined by 3DTEE was corrected for PR by calculation of ELI, there was a further increase (0.52 ± 0.03 cm(2) /m(2) ; P < 0.001), and 10/36 (27.8%) patients were reclassified to moderate AS. CONCLUSION: Three-dimensional TEE is more accurate than 2DTTE and 2DTEE for determining LVOT and AA dimensions. When AS severity is determined by 3DTEE and corrected for PR using the 3D values, it needs to be reclassified from severe to moderate in almost a third of patients.