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Left ventricular hypertrophy (LVH) was one of the earliest studied echocardiographic characteristics of the left ventricle. As the myriad of measurable metrics has multiplied over recent years, this reliable and relevant variable can often be overlooked. In this paper, we discuss appropriate techniques for accurate analysis, underlying pathophysiology, and the contributions from various risk factors. The prognostic implications of LVH on stroke, serious arrhythmias, and sudden cardiac death are reviewed. Finally, we examine the effect of therapy to reduce LVH and the resultant clinical outcomes.

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Cardiac valvular disease as consequence of radiation and chemotherapy during treatment for malignancy is growing in its awareness. While the overwhelming emphasis in this population has been on the monitoring and preservation of left ventricular systolic function, we are now developing a greater appreciation for the plethora of cardiac sequelae beyond this basic model. To this end many institutions across the country have developed cardio-oncology programs, which are collaborative practices between oncologists and cardiologists in order to minimize a patient's cardiovascular risk while allowing them to receive the necessary treatment for their cancer. These programs also help to recognize early nuanced treatment complications such as valvular heart disease, and provide consultation for the most appropriate course of action. In this article we will discuss the etiology, prevalence, diagnosis, and current treatment options of valvular heart disease as the result of chemotherapy and radiation.

Recent therapeutic trials regarding the management of acute heart failure (AHF) failed to demonstrate the efficacy of newer therapeutic modalities and agents. Low-versus high-dose and continuous administration of furosemide were shown not to matter. Ultrafiltration was not found to be more efficacious than sophisticated diuretic therapy including dose-adjusted intravenous furosemide and metolazone. Dopamine and nesiritide were not shown to be superior to current therapy. Tezosentan and tovalptan had no effect on mortality. The development of rolofylline was terminated due to adverse effect (seizures). Lastly, preliminary experience with serelaxin indicates a mortality improvement at six months that remains to be confirmed. The disappointing findings of these recent trials may reflect the lack of efficacy of newer therapeutic modalities and agents. Alternatively the disappointing findings of these recent trials may be in part due to methodological issues. The AHF syndrome is complex with many clinical phenotypes. Failure to match clinical phenotypes and therapeutic modalities is likely to be partly responsible for the disappointing findings of recent AHF trials.

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Purpose of review Preeclampsia complicates 3–5% of first and 15% of subsequent pregnancies. This study reviews the evidence of increase cardiovascular risk in these women. Recent findings Women with preeclampsia are at two-fold higher risk for development of coronary artery disease, stroke and death, and four-fold increased risk of heart failure. Preeclampsia developed in early part of pregnancy confers greater risk than later in pregnancy. Common factors that predispose women to preeclampsia also confer high risk for developing cardiovascular disease include obesity, metabolic abnormalities, dyslipidaemia, insulin resistance, heightened inflammatory responses, hypercoagulable states and endothelia dysfunction. Summary Patients with preeclampsia should be screened at regular intervals by a preventive cardiologist and treated accordingly.