Pulmonary arterial and pulmonary venous hypertension develop from distinctly different etiologies. Pulmonary arterial hypertension (PAH), or Group 1 pulmonary hypertension (PH), is a precapillary PH that arises idiopathically or as the result of a divergent array of causes, including connective tissue disease. Pulmonary venous hypertension (PVH), or Group 2 PH, primarily manifests as a postcapillary PH in the setting of left heart failure or valvular disease. A subset of PVH patients, however, develop a reactive precapillary component of PH that mimics PAH. These patients can be misdiagnosed as having Group 1 PH by 2-dimensional echocardiography and are sometimes treated as such, which leads to exacerbation of heart failure. Therefore, 2-dimensional or Doppler echocardiography alone cannot be used to differentiate between these two classifications of PH. This highlights the need for right heart catheterization in the clinical assessment and diagnostic work-up of PH. The combination of imaging and invasive hemodynamic assessment by right heart catheterization provides the best diagnostic approach to ensure proper delineation of pulmonary arterial and pulmonary venous hypertension, and in turn leads to appropriate treatment.

Pulmonary hypertension, which may lead to right ventricular (RV) failure, increases with left ventricular (LV) diastolic dysfunction severity. The prevalence and determinants of RV failure were analyzed in 120 patients admitted with acute left heart (LH) failure. Patients were divided into RV failure (n=50) and non-RV failure (n=70) groups. The prevalence of RV failure was found to be 42%. In both groups, two thirds of the patients had isolated LV diastolic dysfunction and the rest had combined LV systolic and diastolic dysfunction. Patients in the RV failure group were characterized by higher LV diastolic grade (2.2 ± 0.6 vs 1.84 ± 0.7; P=.0070), pulmonary artery systolic pressure (PASP; 57.8 ± 15.3 vs 50.14 ± 12.1 mm Hg; P=.0028), right atrial enlargement (92% vs 25.7%; P=.000001), and more-than-moderate tricuspid regurgitation (58% vs 27.1%; P=.0006). RV failure is a frequent finding in patients with advanced LH failure. It is strongly associated with the severity of LV diastolic dysfunction and the severity of PASP.

Methylphenidate is a potent central nervous system stimulant that exerts its effects by increasing synaptic levels of dopamine and norepinephrine. It has become key to treating attention deficit-hyperactivity disorder (ADHD) in children and adolescents. As the use of stimulant medications has ballooned in the past decade, so too has awareness of the cardiovascular complications of these drugs. Effects on heart rate and blood pressure as well as tachyarrhythmias have been well described. However, acute cardiomyopathy and pericarditis secondary to methylphenidate use has been rarely reported. We report the case of a 17-year-old male who developed chest pain, elevated cardiac biomarkers, and acute left ventricular dysfunction following a single dose of methylphenidate. The risk of cardiomyopathy in the setting of methylphenidate treatment should prompt further study on the safety of this drug, and lead to ways of identifying those at risk of developing these complications.

No abstract

The development of acute kidney injury in patients with pulmonary embolism (PE) has not been well documented. We report a patient who developed acute oliguria in the setting of massive PE. Catheter embolectomy followed by ultrafiltration resulted in an immediate and dramatic improvement in urine output. Uncharacteristically, serum creatinine did not rise during the oliguric phase for several days until after embolectomy, and there were no metabolic derangements. Our observation that embolectomy and ultrafiltration helped with hemodynamics and renal perfusion despite decreased cardiac output suggests that right ventricular failure from both pressure and volume overload may have been central to this process. We review the older and recent literature in support of our observations.