BackgroundIbrutinib is a tyrosine kinase inhibitor most commonly associated with atrial fibrillation. However, additional cardiotoxicities have been identified, including accelerated hypertension. The incidence and risk factors of new or worsening hypertension following ibrutinib treatment are not as well known.MethodsWe conducted a retrospective study of 144 patients diagnosed with B cell malignancies treated with ibrutinib (n=93) versus conventional chemoimmunotherapy (n=51) and evaluated their effects on blood pressure at 1, 2, 3 and 6 months after treatment initiation. Descriptive statistics were used to compare baseline characteristics for each treatment group. Fisher’s exact test was used to identify covariates significantly associated with the development of hypertension. Repeated measures analyses were conducted to analyse longitudinal blood pressure changes.ResultsBoth treatments had similar prevalence of baseline hypertension at 63.4% and 66.7%, respectively. There were no differences between treatments by age, sex and baseline cardiac comorbidities. Both systolic and diastolic blood pressure significantly increased over time with ibrutinib compared with baseline, whereas conventional chemoimmunotherapy was not associated with significant changes in blood pressure. Baseline hypertensive status did not affect the degree of blood pressure change over time. A significant increase in systolic blood pressure (defined as more than 10 mm Hg) was noted for ibrutinib (36.6%) compared with conventional chemoimmunotherapy (7.9%) at 1 month after treatment initiation. Despite being hypertensive at follow-up, 61.2% of patients who were treated with ibrutinib did not receive adequate blood pressure management (increase or addition of blood pressure medications). Within the ibrutinib group, of patients who developed more than 20 mm Hg increase in systolic blood pressure, only 52.9% had hypertension management changes.ConclusionsIbrutinib is associated with the development of hypertension and worsening of blood pressure. Cardiologists and oncologists must be aware of this cardiotoxicity to allow timely management of blood pressure elevations.
Atrial septal defects (ASD) is a common congenital abnormality discovered in adulthood but ostium primum ASDs are more rare with an incidence of w15% of ASDs.2 ASDs with coexisting pulmonary valve stenosis is rare but has been described in Noonan Syndrome.1 About 66% of Noonan Syndrome patients exhibit congenital heart defects.3,4 ASDs and coexisting valvular pulmonary stenosis in the absence of Noonan syndrome is very rare. CASE PRESENTATION: 62 year-old Hispanic male with CAD with prior PCI, hypertension, and hypothyroidism who presented with progressive dyspnea and palpitations. He was found to be in new-onset atrial fibrillation with ventricular rates in the 160's BPM. Labs revealed normal electrolytes and TSH, elevated BNP (1226pg/ml), and negative troponin-I. CXR was unremarkable. He was rate controlled, anti-coagulated, and underwent successful TEE with 200J of DCCV with restoration of sinus rhythm. His TEE showed a normal EF but a RA measuring 5.1cm (ID) in end-systole along with a membrane in the posterior aspect of the RA (prominent eustachian valve versus cor triatriatum dextrum), mildly dilated RV, mild MR, and a large primum ASD measuring 4.91cm2 by planimetry. A TTE (in sinus rhythm) showed mild-mod pulmonary stenosis and mild pulmonary regurgitation by doppler (mean systolic gradient 17.00mmHg, peak systolic gradient 30.00mmHg) along with dilated pulmonary arteries with possible flow reversal in the right pulmonary artery. Left heart cath showed non-obstructive CAD. CTA of the pulmonary veins showed no anomalous pulmonary vein return but did show a 32mm main pulm vein, 42mm left pulm artery, 28mm right pulm artery, and known ASD measuring 24x30mm. He remained in sinus rhythm and was discharged.
Introduction: Right ventricular failure (RVF) and ventricular tachyarrhythmias (VA) are common causes of poor outcome and mortality in patients with left ventricular assist device (LVAD). VA can precipitate RVF and inotropic therapy can further exacerbate VA. The purpose of this observational study was to investigate the individual and combined impact of RVF and VA on mortality in the early postoperative period after LVAD. Methods: We performed a retrospective analysis of patients undergoing implantation of an LVAD between 2014 to 2017 (N=110). Telemetry tracings and device interrogations were reviewed. Early VA was defined as any ventricular tachycardia and ventricular fibrillation within the first month after LVAD associated with hemodynamic compromise that required device therapy, catheter ablation, and/or antiarrhythmic therapy. Kaplan-Meier statistics with the Mantel-Cox log-rank test was used to analyze survival. Results: We identified 110 LVAD patients, age 57±13 years, 80 males (73%), ischemic cardiomyopathy n=54 (49%), (HeartWare (n=44), HeartMate II (n=44), and HeartMate III (n=22)). Patients were categorized into group A - early VA and severe RVF (n=14); group B - early VA without RVF (n=16); group C - severe RVF without early VA (n=33); and group D - neither VA nor RVF (n=47). The 1-year survival of group A, B, C, and D was 50%, 69%, 73%, and 89%, respectively (p=0.001 comparing each group to the other groups, enclosed figure). The presence of early VA did not relate to RVF (p=0.7). Pre-operative VA was related to post-LVAD VA (RR 9.4, p=0.003). Conclusions: Patients without early VA or severe RVF demonstrated the best survival. Both, VA and severe RVF decreased survival. The presence of both, VA and RVF appears to potentiate mortality. Pre-operative VA is related to post-LVAD VA. These data raise the question if intra-operative ablative therapy in patients undergoing LVAD implantation could improve post-operative mortality, VA, and RVF.
Background: Coronary artery calcium (CAC) scoring is an important tool for cardiovascular risk stratification. CAC scoring in both asymptomatic and symptomatic, low-intermediate risk patients has also shown prognostic utility and has a high negative predictive value for obstructive coronary artery disease (CAD). Patients who present with chest pain frequently undergo non-gated chest computed tomography (CT) to evaluate for non-cardiac etiologies. In fact, several studies have demonstrated that a CAC score from a non-gated chest CT correlates well with a dedicated calcium-scoring CT. However, the predictive value on CAD through assessing the presence (CAC>0) or the absence of calcium (CAC=0) detected on non-gated chest CT in patients presenting with chest pain is unknown. Methods: Low-intermediate risk patients (n=92) presenting to the emergency department with chest pain who underwent non-gated chest CT and were subsequently evaluated with either a cardiac stress test or invasive coronary angiography were included. Dichotomous CAC was assessed in a blinded fashion and classified as CAC=0 or CAC>0. Obstructive CAD was defined as either: ischemia on stress testing or any coronary artery stenosis greater than 70% (left main coronary artery stenosis greater than 50%) on invasive coronary angiography. Results: CAC=0 on non-gated chest CT was found in 59.2% (n=42). Patients with CAC=0 had a significantly lower age and TIMI score compared to patients with a CAC>0. (p<0.01 ) Patients with a CAC>0 were found to more likely have obstructive CAD on subsequent testing: cardiac stress test (Likelihood ratio[LR]:6.42, p=0.022); and invasive angiography (LR:12.46, p=0.002). There were no patients with a CAC=0 that were found to have obstructive CAD on invasive coronary angiography, resulting in a 100% sensitivity and 100% negative predictive value. Conclusion: Patient who presents with chest pain frequently undergo evaluation with a non-gated chest CT to assess non-cardiac etiologies. Exclusion of CAC on non-gated chest CT may be useful as an adjunct for further risk stratification to avoid potential adverse events and cost associated with further testing.
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