Browsing by Author "Bashore, Thomas M"
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Item Open Access Addressing the Menace of Enterococcal Endocarditis.(Journal of the American College of Cardiology, 2020-02) Bashore, Thomas M; Turner, Nicholas AItem Open Access Association of anemia and long-term survival in patients with pulmonary hypertension.(Int J Cardiol, 2011-08-04) Krasuski, Richard A; Hart, Stephen A; Smith, Brad; Wang, Andrew; Harrison, J Kevin; Bashore, Thomas MBACKGROUND: Anemia is a marker of worsened clinical outcome in patients with heart failure from left ventricular dysfunction. Pulmonary hypertension often results in right ventricular dysfunction. Accordingly we sought to examine the association of hemoglobin levels and long-term all-cause mortality in a cohort of patients with pulmonary hypertension. METHODS: Baseline demographic information, clinical characteristics and fasting blood work were obtained in a cohort of 145 patients with pulmonary hypertension referred for pulmonary vasodilator testing. Data was retrospectively analyzed with Cox-proportional hazards analysis. RESULTS: Baseline characteristics of the cohort included age (mean±SD) 55.8±14.6 years, 75% women, 50% with idiopathic pulmonary hypertension, mean pulmonary artery pressure 46.1±14.2 mm Hg and arterial O(2) saturation 91±6 %. The most commonly utilized pulmonary hypertension specific therapeutic agents in descending order of frequency were epoprostenol (27%), sildenafil (21%), bosentan (17%), and treprostinil (6%). Over a median follow-up of 2.1 years, there were 39 deaths (26.9%). Patients who died had significantly lower hemoglobin levels than those survived (12.2±2.3 vs. 13.7±2.0, p<0.001). After adjustment for known predictors of death and pulmonary hypertension etiology, anemic patients were 3.3 times more likely to die than non-anemic patients (95% CI [1.43-7.51], p=0.005). CONCLUSIONS: Hemoglobin levels closely parallel survival in pulmonary hypertension. Modification of anemia in this disorder could alter the clinical course and calls for further research in this area.Item Unknown Congenital Heart Disease Epidemiology in the United States: Blindly Feeling for the Charging Elephant.(Circulation, 2016-07-12) Krasuski, Richard A; Bashore, Thomas MItem Unknown Effect of Patent Foramen Ovale in Patients With Pulmonary Hypertension.(The American journal of cardiology, 2018-08) Sharan, Lauren; Stackhouse, Kathryn; Awerbach, Jordan D; Bashore, Thomas M; Krasuski, Richard ASeptostomy reduces right ventricular (RV) workload at the expense of hypoxemia in patients with advanced pulmonary hypertension (PH). A patent foramen ovale (PFO) may serve as a "natural" septostomy, but the incidence and impact of a PFO in PH remains uncertain. We prospectively examined echocardiograms in 404 PH patients referred for initial hemodynamic assessment. Patients included had saline bubble injection and if negative repeatinjection after Valsalva maneuver. Echocardiographic and hemodynamic data were examined. Survival was modeled using Kaplan-Meier method. Eisenmenger syndrome or known atrial shunts other than PFO were excluded: 292 patients met entry criteria. A PFO was identified in 16.8% of the entire cohort, 22.9% of pulmonary arterial hypertension (PAH) patients, and 8.6% of Dana Point group 2 PH patients. Right atrial to pulmonary capillary wedge pressure difference was lowest in the latter group (-7.9 ± 7.1 vs -1.7 ± 5.5 mm Hg for all others, p <0.01). Patients with a PFO were younger (53.9 vs 58.6 years, p = 0.02). A PFO was more often present with moderately or severely dilated (p = 0.01) or dysfunctional (p = 0.03) RVs. Six year survival was unchanged by PFO presence for all patients, including those with PAH. Proportional hazards analysis found only age and functional class independently predicted survival (p <0.01). A PFO is identified less often in Dana Point group 2 PH, likely due to inability of Valsalva maneuver to overcome right atrial to pulmonary capillary wedge pressure difference. In conclusion, the incidence of a PFO in the PH population increases with more dilated and dysfunctional RVs, suggesting that the PFO may be stretched open rather than congenital. The presence of a PFO does not impact survival in PH or PAH.Item Unknown Health insurance and racial disparities in pulmonary hypertension outcomes.(Am J Manag Care, 2017-08) Parikh, Kishan S; Stackhouse, Kathryn A; Hart, Stephen A; Bashore, Thomas M; Krasuski, Richard AOBJECTIVES: Pulmonary hypertension portends a poorer prognosis for blacks versus white populations, but the underlying reasons are poorly understood. We investigated associations of disease characteristics, insurance status, and race with clinical outcomes. STUDY DESIGN: Retrospective cohort study of patients presenting for initial pulmonary hypertension evaluation at 2 academic referral centers. METHODS: We recorded insurance status (Medicare, Medicaid, private, self-pay), echocardiographic, and hemodynamics data from 261 patients (79% whites, 17% blacks) with a new diagnosis of pulmonary hypertension. Subjects were followed for 2.3 years for survival. Adjustment for covariates was performed with Cox proportional hazards modeling. RESULTS: Compared with white patients, blacks were younger (50 ± 15 vs 53 ± 12 years; P = .04), with females representing a majority of patients in both groups (80% vs 66%; P = .08) and similar functional class distribution (class 2/3/4: 30%/52%/16% blacks vs 33%/48%/14% whites; P = .69). Blacks diagnosed with incident pulmonary hypertension were more frequently covered by Medicaid (12.5% vs 0.7%) and had less private insurance (50% vs 61%; P = .007) than whites. At presentation, blacks had more right ventricular dysfunction (P = .04), but similar mean pulmonary arterial pressure (46 vs 45 mm Hg, respectively; P = .66). After adjusting for age and functional class, blacks had greater mortality risk (hazard ratio [HR], 2.06; 95% confidence interval [CI], 1.18-3.44), which did not differ by race after additional adjustment for insurance status (HR, 1.74; 95% CI, 0.84-3.32; P =.13). CONCLUSIONS: In a large cohort of patients with incident pulmonary hypertension, black patients had poorer right-side heart function and survival rates than white patients. However, adjustment for insurance status in our cohort removed differences in survival by race.Item Unknown Impact of diabetes in patients with pulmonary hypertension.(Pulmonary circulation, 2015-03) Abernethy, Abraham D; Stackhouse, Kathryn; Hart, Stephen; Devendra, Ganesh; Bashore, Thomas M; Dweik, Raed; Krasuski, Richard ADiabetes complicates management in a number of disease states and adversely impacts survival; how diabetes affects patients with pulmonary hypertension (PH) has not been well characterized. With insulin resistance having recently been demonstrated in PH, we sought to examine the impact of diabetes in these patients. Demographic characteristics, echo data, and invasive hemodynamic data were prospectively collected for 261 patients with PH referred for initial hemodynamic assessment. Diabetes was defined as documented insulin resistance or treatment with antidiabetic medications. Fifty-five patients (21%) had diabetes, and compared with nondiabetic patients, they were older (mean years ± SD, 61 ± 13 vs. 56 ± 16; [Formula: see text]), more likely to be black (29% vs. 14%; [Formula: see text]) and hypertensive (71% vs. 30%; [Formula: see text]), and had higher mean (±SD) serum creatinine levels (1.1 ± 0.5 vs. 1.0 ± 0.4; [Formula: see text]). Diabetic patients had similar World Health Organization functional class at presentation but were more likely to have pulmonary venous etiology of PH (24% vs. 10%; [Formula: see text]). Echo findings, including biventricular function, tricuspid regurgitation, and pressure estimates were similar. Invasive pulmonary pressures and cardiac output were similar, but right atrial pressure was appreciably higher (14 ± 8 mmHg vs. 10 ± 5 mmHg; [Formula: see text]). Despite similar management, survival was markedly worse and remained so after statistical adjustment. In summary, diabetic patients referred for assessment of PH were more likely to have pulmonary venous disease than nondiabetic patients with PH, with hemodynamics suggesting greater right-sided diastolic dysfunction. The markedly worse survival in these patients merits further study.Item Unknown Pulmonary hypertension and elevated transpulmonary gradient in patients with mitral stenosis.(J Heart Valve Dis, 2010-11) Hart, Stephen A; Krasuski, Richard A; Wang, Andrew; Kisslo, Katherine; Harrison, J Kevin; Bashore, Thomas MBACKGROUND AND AIM OF THE STUDY: Pulmonary hypertension frequently complicates mitral stenosis, with a subset of these patients exhibiting pressures well in excess of their mitral valve hemodynamics. The prevalence of this condition and its impact on clinical outcome following percutaneous balloon mitral commissurotomy (PBMC) is unknown. METHODS: The transpulmonary gradient (TPG) was measured in 317 patients undergoing PBMC; patients were subsequently defined as having either an appropriate or excessive TPG (< or =15 mmHg or >15 mmHg, respectively). Twenty-two patients were excluded due to valvuloplasty-related significant mitral regurgitation. The remaining 295 patients (250 females, 45 males; mean age 52 +/- 13 years) were prospectively followed up, with each patient underwent serial echocardiography. RESULTS: Among the patients, 214 (73%) had pulmonary hypertension (pulmonary artery pressure >25 mmHg) and 55 (19%) also had an elevated TPG. Females were almost fivefold more likely than males to have an elevated TPG (p = 0.003). Patients with an elevated TPG had a worse mean NYHA functional class than those with a normal TPG (3.0 +/- 0.5 versus 2.7 +/- 0.6, p = 0.01), while the mitral valve area (MVA) was slightly smaller in patients with an elevated TPG (1.0 +/- 0.2 versus 1.1 +/- 0.2 cm2, p = 0.003). All patients demonstrated a significant increase in MVA after commissurotomy (final MVA 1.7 +/- 0.6 cm2, p < 0.001 for elevated TPG; 1.8 +/- 0.4 cm2, p < 0.001 for normal TPG), and the NYHA class at six months was improved for all patients (2.8 +/- 0.6 versus 1.6 +/- 0.7, p < 0.001). The improvements in NYHA class, TPG and MVA were sustained at 36 months. CONCLUSION: Pulmonary hypertension with elevated TPG occurs in patients with mitral stenosis, and is significantly more common in females. Despite worse symptoms and higher right-sided pressures, PBMC is equally successful in patients with a normal TPG, and provides sustained benefit for up to 36 months after the procedure.Item Unknown Response to inhaled nitric oxide predicts survival in patients with pulmonary hypertension.(J Card Fail, 2011-04) Krasuski, Richard A; Devendra, Ganesh P; Hart, Stephen A; Wang, Andrew; Harrison, J Kevin; Bashore, Thomas MOBJECTIVE: To examine the ability of vasodilator response to predict survival in a diverse cohort of patients with pulmonary hypertension (PH). PATIENTS & METHODS: A total of 214 consecutive treatment-naive patients referred for invasive PH evaluation were enrolled between November 1998 and December 2008. Vasoreactivity was assessed during inhalation of 40 parts per million nitric oxide (iNO) and vasodilator responders were defined as those participants who achieved a mean pulmonary artery pressure (PAP) of ≤ 40 mm Hg and a drop in mean PAP ≥ the median for the cohort (13%). Kaplan-Meier analysis and Cox proportional hazards modeling were used to identify predictors of survival. RESULTS: There were 51 deaths (25.9%) over a mean follow-up period of 2.3 years. Kaplan-Meier analysis demonstrated that vasodilator responders had significantly improved survival (P < .01). Vasodilator responders had improved survival regardless of whether or not they had idiopathic or nonidiopathic PH (P = .02, P < .01) or whether or not they had Dana Point class 1 or non-Dana Point class 1 PH (P < .01, P = .01). In multivariate modeling, advanced age, elevated right atrial pressure, elevated serum creatinine, and worsened functional class significantly predicted shorter survival (P = .01, P = .01, P = .01, P < .01), whereas vasodilator response predicted improved survival (P = .01). CONCLUSIONS: Vasodilator responsiveness to iNO is an important method of risk stratifying PH patients, with results that apply regardless of clinical etiology.