In Reply: I agree with Mssrs Dittmar and Weller that there is a trade-off between medical jargon and vernacular language. All professions develop their own language out of necessity to communicate with colleagues quickly and to protect themselves from outsiders. It may not always be possible to make concepts more understandable for patients without sacrificing brevity or specificity. However, I disagree that clinicians are the only target audience of documentation in the electronic era, given that many health care institutions are making tethered personalized health records available to their patients. I mentioned in the article that to make any terminology accurate and appropriate for communication, "[p]erhaps it is time for medical scholars to work with consumers to define the most helpful terms for patients and families."Moreover, not all current medical jargon is useful for clinicians or patients. For example, wheezing is a more specific and helpful term than rhonchi. Most patients with asthma would have had wheezing explained to them but not rhonchi, and not all medical practitioners can precisely define the term rhonchi when this is communicated to them by their colleagues. Terminology would also need to be updated periodically-indeed, some existing medical terms are outdated because of changes in our understanding of disease mechanisms.As therapeutic advances reach patients, motivating patients to adhere to recommended regimens may represent "the last mile" of health care delivery. To help patients understand their disease processes and participate in shared decision making, physicians must speak the patient's language whenever possible.The Accreditation Council for Graduate Medical Education endorses interpersonal and communications skills as a core competency, 1 and in the electronic era, this may include online communications. Patients who look up medical terms online may encounter more medical jargon that they may not be able to interpret due to limited health literacy. I hope that by making medical language less mysterious, physicians can allow patients to have more meaningful participation in their own health care. The purpose of my Viewpoint was to start this conversation. It is time to revamp the arcane system of health communications in the electronic era when many patients can use these tools to access health-related information.

Pulmonary arterial hypertension (PH) and chronic kidney disease (CKD) both profoundly impact patient outcomes, whether as primary disease states or as co-morbid conditions. PH is a common co-morbidity in CKD and vice versa. A growing body of literature describes the epidemiology of PH secondary to chronic kidney disease and end-stage renal disease (ESRD) (WHO group 5 PH). But, there are only limited data on the epidemiology of kidney disease in group 1 PH (pulmonary arterial hypertension [PAH]). The purpose of this review is to summarize the current data on epidemiology and discuss potential disease mechanisms and management implications of kidney dysfunction in PAH. Kidney dysfunction, determined by serum creatinine or estimated glomerular filtration rate, is a frequent co-morbidity in PAH and impaired kidney function is a strong and independent predictor of mortality. Potential mechanisms of PAH affecting the kidneys are increased venous congestion, decreased cardiac output, and neurohormonal activation. On a molecular level, increased TGF-β signaling and increased levels of circulating cytokines could have the potential to worsen kidney function. Nephrotoxicity does not seem to be a common side effect of PAH-targeted therapy. Treatment implications for kidney disease in PAH include glycemic control, lifestyle modification, and potentially Renin-Angiotensin-Aldosterone System (RAAS) blockade.

Pulmonary hypertension (PH) is common in patients with chronic kidney disease (CKD) and associated with increased mortality but the hemodynamic profiles, clinical risk factors, and outcomes have not been well characterized. Our objective was to define the hemodynamic profile and related risk factors for PH in CKD patients. We extracted clinical and hemodynamic data from Vanderbilt’s de-identified electronic medical record on all patients undergoing right heart catheterization during 1998–2014. CKD (stages III–V) was defined by estimated glomerular filtration rate thresholds. PH was defined as mean pulmonary pressure ≥ 25 mmHg and categorized into pre-capillary and post-capillary according to consensus recommendations. In total, 4635 patients underwent catheterization: 1873 (40%) had CKD; 1518 (33%) stage 3, 230 (5%) stage 4, and 125 (3%) stage 5. PH was present in 1267 (68%) of these patients. Post-capillary (n = 965, 76%) was the predominant PH phenotype among CKD patients versus 302 (24%) for pre-capillary (P < 0.001). CKD was independently associated with pulmonary hypertension (odds ratio = 1.4, 95% confidence interval = 1.18–1.65). Mortality among CKD patients rose with worsening stage and was significantly increased by PH status. PH is common and independently associated with mortality among CKD patients referred for right heart catheterization. Post-capillary was the most common etiology of PH. These data suggest that PH is an important prognostic co-morbidity among CKD patients and that CKD itself may have a role in the development of pulmonary vascular disease in some patients.

BackgroundTransthoracic echocardiography (TTE) is used to estimate pulmonary artery systolic pressure, but an adequate tricuspid regurgitation velocity (TRV) needed to calculate pulmonary artery systolic pressure is not always present. It is unknown whether the absence of a measurable TRV signifies normal pulmonary artery pressure.Methods and ResultsWe extracted hemodynamic, TTE, and clinical data from Vanderbilt's deidentified electronic medical record in all patients referred for right heart catheterization between 1998 and 2014. Pulmonary hypertension (PH) was defined as mean pulmonary artery pressure ≥25 mm Hg. We examined the prevalence and clinical correlates of PH in patients without a reported TRV. We identified 1262 patients with a TTE within 2 days of right heart catheterization. In total, 803/1262 (64%) had a reported TRV, whereas 459 (36%) had no reported TRV. Invasively confirmed PH was present in 47% of patients without a reported TRV versus 68% in those with a reported TRV (P<0.001). Absence of a TRV yielded a negative predictive value for excluding PH of 53%. Right ventricular dysfunction, left atrial dimension, elevated body mass index, higher brain natriuretic peptide, diabetes mellitus, and heart failure were independently associated with PH among patients without a reported TRV.Conclusions PH is present in almost half of patients without a measurable TRV who are referred for both TTE and right heart catheterization. Clinical and echocardiographic features of left heart disease are associated with invasively confirmed PH in subjects without a reported TRV. Clinicians should use caution when making assumptions about PH status in the absence of a measurable TRV on TTE.

BackgroundBlood pressure (BP) guidelines for patients with aortic stenosis or a history of aortic stenosis treated with aortic valve replacement (AVR) match those in the general population, but this extrapolation may not be warranted.Methods and ResultsAmong patients enrolled in the Medtronic intermediate, high, and extreme risk trials, we included those with a transcatheter AVR (n=1794) or surgical AVR (n=1103) who were alive at 30 days. The associations between early (average of discharge and 30 day post‐AVR) systolic BP (SBP) and diastolic BP (DBP) measurements and clinical outcomes between 30 days and 1 year were evaluated. Among 2897 patients, after adjustment, spline curves demonstrated an association between lower SBP (<120 mm Hg, representing 21% of patients) and DBP (<60 mm Hg, representing 30% of patients) and increased all‐cause and cardiovascular mortality and repeat hospitalization. These relationships were unchanged when patients with moderate‐to‐severe aortic regurgitation post‐AVR were excluded. After adjustment, compared with DBP 60 to <80 mm Hg, DBP 30 to <60 mm Hg was associated with increased all‐cause (adjusted hazard ratio 1.62, 95% CI 1.23–2.14) and cardiovascular mortality (adjusted hazard ratio 2.13, 95% CI 1.52–3.00), but DBP 80 to <100 mm Hg was not. Similarly, after adjustment, compared with SBP 120 to <150 mm Hg, SBP 90 to <120 mm Hg was associated with increased all‐cause (adjusted hazard ratio 1.63, 95% CI 1.21–2.21) and cardiovascular mortality (adjusted hazard ratio 1.81, 95% CI 1.25–2.61), but SBP 150 to <180 mm Hg was not.ConclusionsLower BP in the first month after transcatheter AVR or surgical AVR is common and associated with increased mortality and repeat hospitalization. Clarifying optimal BP targets in these patients ought to be a priority and may improve patient outcomes.Clinical Trial Registration InformationURL: http://www.clinicaltrials.gov. Unique identifiers: NCT01586910, NCT01240902.