Ventricular hypertrophy is an ominous escalation of hemodynamically stressful conditions such as hypertension and valve disease. The pathophysiology of hypertrophy is complex and multifactorial, as it touches on several cellular and molecular systems. Understanding the molecular background of cardiac hypertrophy is essential in order to protect the myocardium from pathological remodeling, or slow down the destined progression to heart failure. In this review we highlight the most important molecular aspects of cardiac hypertrophic growth in light of the currently available published research data.

Papillary renal cell carcinoma (PRCC) has 2 histologic subtypes. Almost half of the cases fail to meet all morphologic criteria for either type, hence are characterized as PRCC not otherwise specified (NOS). There are yet no markers to resolve the PRCC NOS category. Accurate classification can better guide the management of these patients. In our previous PRCC study we identified markers that can distinguish between the subtypes. A PRCC patient cohort of 108 cases was selected for the current study. A panel of potentially distinguishing markers was chosen from our previous genomic analysis, and assessed by immunohistochemistry. The panel exhibited distinct staining patterns between the 2 classic PRCC subtypes; and successfully reclassified the NOS (45%) cases. Moreover, these immunomarkers revealed a third subtype, PRCC3 (35% of the cohort). Molecular testing using miRNA expression and copy number variation analysis confirmed the presence of 3 distinct molecular signatures corresponding to the 3 subtypes. Disease-free survival was significantly enhanced in PRCC1 versus 2 and 3 (P=0.047) on univariate analysis. The subtypes stratification was also significant on multivariate analysis (P=0.025; hazard ratio, 6; 95% confidence interval, 1.25-32.2). We propose a new classification system of PRCC integrating morphologic, immunophenotypical, and molecular analysis. The newly described PRCC3 has overlapping morphology between PRCC1 and PRCC2, hence would be subtyped as NOS in the current classification. Molecularly PRCC3 has a distinct signature and clinically it behaves similar to PRCC2. The new classification stratifies PRCC patients into clinically relevant subgroups and has significant implications on the management of PRCC.

Right ventricular failure (RVF) is an unfortunate complication that continues to limit outcomes following durable left ventricular assist device (LVAD) implantation. Despite several ‘RVF risk scores’ having been proposed, preoperative prediction of post-LVAD RVF remains a guesstimate at best. Current strategies for institution of temporary RVAD support are invasive, necessitate additional re-thoracotomy, restrict postoperative mobilization, and/or entail prolonged retention of prosthetic material in-situ. The authors propose a novel surgical strategy comprising simultaneous implantation of a permanent LVAD and percutaneous TandemHeart® plus ProtekDuo® to provide temporary RVAD support and preempt RVF in patients with impaired RV function.

Aims The occurrence of hyperbilirubinaemia after heart surgery using cardiopulmonary bypass or post‐operative heart failure is fairly common. We investigated the incidence, predictive value, and post‐operative outcome of hyperbilirubinaemia after cardiac surgery in an effort to identify potential risk factors and significance on clinical outcome. Methods and results Between 2006 and 2016, 1272 (10.1%) out of 12 556 patients developed hyperbilirubinaemia, defined as bilirubin concentration >3 mg/dL, during post‐operative course at our institution. All patients who were operated using cardiopulmonary bypass were included. Hepatic dysfunction was diagnosed preoperatively in 200 patients (15.7%), whereas mean model of end‐stage liver disease score was 11.22 ± 4.99. Early mortality was 17.4% with age [hazard ratio (HR) 1.019, 95% confidence interval (CI) 1.008–1.029; P = 0.001], diabetes (HR 1.115, CI 1.020–1.220; P = 0.017), and emergent procedures (HR 1.315, CI 1.012–1.710) as multivariate predictors. Post‐operative predictors were low‐output syndrome (HR 3.193, 95% CI 2.495–4.086; P < 0.001), blood transfusion (HR 1.0, CI 1.0–1.0; P < 0.001), and time to peak bilirubin (HR 1.1, CI 1.0–1.1; P < 0.001). We found an increased correlation with mortality at 3.5 post‐operative day as well as an optimal cut‐off value for bilirubin of 5.35 mg/dL. A maximum bilirubin of 25.5 mg/dL was associated with 99% mortality. Survival analysis showed significantly decreased survival for patients who developed late, rather than early, hyperbilirubinaemia. Conclusions Post‐operative hyperbilirubinaemia is a prevalent threat after cardiopulmonary bypass, associated with high early mortality. The timing and amount of peak bilirubin concentration are linked to the underlying pathology and are predictors of post‐operative outcome. Patients with late development of steep hyperbilirubinaemia warrant meticulous post‐operative care optimizing cardiac and end organ functions before reaching the point of no return.