Case report of a coronary artery-right ventricular fistula following repeat endomyocardial biopsies in a heart transplant patient.

BACKGROUND: Endomyocardial biopsy (EMB) remains the gold standard for cellular rejection surveillance in heart transplant recipients. Coronary artery fistula formation is a rare late and potentially catastrophic complication of repeated endomyocardial biopsies, without contemporary evidence on incidence or management. CASE SUMMARY: A 47-year-old male was found to have a fistula between his right ventricle and his left anterior descending artery on an angiogram that was performed as a part of regular screening of coronary allograft vasculopathy. Given the low shunt fraction, asymptomatic nature, and lack of guidelines on definitive management, the patient is undergoing conservative management with regular surveillance. DISCUSSION: Coronary artery fistulas were once thought to be rare complications of repeated EMB, but the true prevalence is likely to be higher than previously believed. Ideal treatment and monitoring is unknown given the relative rarity of the condition.

Soluble Urokinase Plasminogen Activator Receptor Is Associated With Subclinical Myocardial Impairment by Speckle Tracking Echocardiography in Lung Cancer Patients.

BACKGROUND: Plasma cardiac biomarkers have emerged as a cost-effective diagnostic tool aimed at early identification of cardiotoxicity. Soluble urokinase plasminogen activator receptor (suPAR) is a bone marrow cell derived signaling molecule that is associated with cardiovascular disease outcomes. OBJECTIVES: We investigated associations between suPAR and global longitudinal strain (GLS) as a marker of early myocardial impairment in lung cancer patients. METHODS: We retrospectively analyzed 52 patients with stage IV non-small cell lung cancer with normal left ventricular ejection fraction (LVEF >55%) and without known heart disease or end-stage renal disease (ESRD). We studied associations between cardiac biomarkers and echocardiographic measures of systolic and diastolic function. GLS was analyzed using 2D speckle-tracking echocardiography via vendor-independent software (TomTec). RESULTS: Median plasma suPAR was 7.0 ng/mL (interquartile range: 5.4-9.0). Mean LVEF was 61.9 ± 8.3% and mean GLS was-19.3 ± 2.1%. Inter-observer reproducibility was excellent for GLS as determined by Intraclass Correlation Coefficient analysis, ICC = 0.81 (0.68-0.89). After multivariate analysis, suPAR was the only biomarker associated with GLS (p = 0.009). suPAR was also associated with diastolic parameters E velocity (p = 0.018), A velocity (p = 0.017), and E/E' ratio (p = 0.033). Interestingly, suPAR was not associated with LVEF (p = 0.916). In addition, suPAR and GLS were found to be age-independent predictors of all-cause mortality, though only GLS remained significant after multivariate adjustment. CONCLUSIONS: In this cohort of stage IV non-small cell lung cancer patients with normal LVEF and without known heart disease or ESRD, suPAR was associated with GLS and diastolic impairment. suPAR is a readily available inexpensive biomarker; further research is required to evaluate the possible role of suPAR in screening for subclinical LV dysfunction in the high-risk oncological population.

Prediction of doxorubicin cardiotoxicity by early detection of subclinical right ventricular dysfunction.

BACKGROUND: Doxorubicin remains one of the most common causes of cardiotoxicity in patients with lymphoma, leading to significant morbidity and mortality. Early decline in left ventricular (LV) ejection fraction predicts chemotherapy-induced cardiotoxicity and mortality, but limited data exist on doxorubicin-induced subclinical right ventricular (RV) dysfunction. We investigated dose-dependent subclinical doxorubicin-induced RV dysfunction in lymphoma patients. METHODS: Thirty-five patients with adult lymphoma treated with doxorubicin were studied. All patients had normal baseline LV ejection fraction (LVEF > 55%), and no known cardiopulmonary disease. We studied the dose-dependent effect of doxorubicin on RV strain by 2D speckle-tracking echocardiography (STE) using a vendor-independent software (TomTec). Images were analyzed offline by two independent observers blinded to the clinical characteristics of the study population. Baseline LVEF, RV fractional area change (RV FAC), RV free wall strain (RV FWS), and RV global longitudinal strain (RV GLS) were measured prior to chemotherapy initiation and compared with echo studies obtained at a 6-month follow-up interval. Patients served as their own controls. Comparisons between pre- and post-therapy were achieved using paired Student's t-tests or Chi-Square test. RESULTS: The Interobserver Intraclass Correlation Coefficient for RV GLS, RV FAC and RV FWS, was 0.87, 0.81 and 0.79, respectively. The mean age was 51 ± 13 years, 40% women, 60% white. The mean cumulative doxorubicin dose was 239 ± 104 mg m- 2. There was there was significant decline in RV FAC (47.3 ± 4.4% vs. 43.7 ± 3.9%), RV FWS (- 24.9 ± 3.3 vs. -22.2 ± 2.9), and RV GLS (- 22.4 ± 4.1 vs. -20.6 ± 3.4) (all p < 0.01); but no significant decline in LVEF during the 6-month follow up (63.3 ± 6.2% vs. 61.6 ± 11.1%, p = 0.374). At cumulative doxorubicin dose ≥200 mg m- 2 we found a significant decline in RV FAC (47.0 ± 4.7% vs. 42.2 ± 3.1%, p < 0.01), RV FWS (- 24.6 ± 3.6 vs. -21.5 ± 2.4, p < 0.01), and RV GLS (- 22.3 ± 4.5 vs. -20.1 ± 2.9, p = 0.03). CONCLUSION: In this cohort of adult lymphoma patients, doxorubicin-based therapy was associated with subclinical RV dysfunction, but not LV dysfunction, at a cumulative dose ≥200 mg m- 2. Additional studies evaluating the long-term prognostic implications of RV dysfunction in this population are essential.

Pulmonary Hypertension and Cancer: Etiology, Diagnosis, and Management.

OPINION STATEMENT: Pulmonary hypertension is caused by cancer and its therapeutic agents including chemotherapy, radiotherapy, and even the targeted therapies. Ironically, some of the cancer therapies that cause one type of pulmonary hypertension (PH) could potentially be employed in the treatment of another PH type. Greater awareness on the role of cancer therapeutic agents in causing PH is required. Conversely, since PH is mostly incurable, the potential role of some of these cancer therapeutic agents in the cure of PH should be recognized. In short, the relationship between cancer, cancer therapy, and PH is an interesting one requiring further attention, education, and research.

Association of passive and active smoking with pre-diabetes risk in a predominantly Hispanic population.

Smoking is the leading cause of avoidable death and is associated with type 2 diabetes (T2D) risk. Previous studies on the impact of passive smoking have not been applied to a Hispanic-majority population. We investigated the association between active smoking, exposure to environmental tobacco smoke (ETS), and pre-diabetes risk in a New Mexico population. We hypothesized that pre-diabetes risk increases with increasing smoking status after adjustment for important covariates. We screened 219 adults from an ongoing study who were categorized according to their smoking status (never smoker, current smoker, previous smoker) and their exposure to ETS (exposed or unexposed). Glucose homeostasis status was assigned using A1c: no diabetes (A1c <5.7%), pre-diabetes (A1c 5.7-6.4%), and T2D (A1c >6.4%). Among 160 patients with complete data, 51.6% had no diabetes and 48.4% had pre-diabetes. The mean age was 44.8±13.5 years. The study population was predominantly female (64.4%), and the ethnic composition was 44.4% Hispanic, 39.4% non-Hispanic White (NHW), 10.6% American Indian, 2.5% African-American, and 3.1% other. Using a logistic model with 2-way interactions, all predicted probabilities for being at risk for pre-diabetes were significant at the 0.001 level for smoking status and ETS exposure after adjusting for age, sex, ethnicity, family history of diabetes, alcohol consumption, BMI, and blood pressure. Active or passive smoking is independently associated with pre-diabetes risk.