A Galvanizing Solution: Colonoscopy Bowel Preparation as a Trigger for Supraventricular Tachycardia.

BACKGROUND: Polyethylene glycol (PEG)-based solutions are among the most commonly used bowel preparation regimens for colonoscopy. Although these solutions are well tolerated, rare adverse cardiac events have been reported. OBJECTIVES: We sought to identify the characteristics that may predispose patients to develop supraventricular tachycardia (SVT) after ingestion of GoLYTELY (PEG 3350 and electrolytes oral solution) in anticipation for their colonoscopy. METHODS: We performed a retrospective observational cohort study of the electronic medical record of all patients who developed SVT after ingestion of GoLYTELY solution from April 2012 to March 2019 at the John D. Dingell VA Medical Center. Clinical data were obtained through review of medical records. RESULTS: We identified 16 patients with new-onset SVT after ingestion of bowel preparation solution before undergoing the colonoscopy procedure. In all, 12 (75%) patients developed atrial fibrillation, 3 (18.8%) patients developed atrial tachycardia, and 1 patient (6.3%) developed atrial flutter. Most patients were male (93.8%), and the mean age was 69 ± 8.2 years. The commonly associated comorbidities were hypertension (87.5%), hyperlipidemia (56.3%), and diabetes (37.5%). Laboratory testing demonstrated a normal electrolyte panel and thyroid stimulating hormone level. A significant percentage of patients had dilated atria and left-ventricular hypertrophy on echocardiogram. CONCLUSION: Our case series suggests that there may be certain individuals who are predisposed to development of atrial arrhythmias, more so than others, after ingestion of PEG based solution for colonoscopy. We hypothesize that the combination of atrial dilation, sympathovagal discharge, and transient electrolyte shifts at the cellular level led to the development of SVTs.

Treatment Failures of Direct Oral Anticoagulants.

BACKGROUND: Use of direct oral anticoagulants (DOACs) has increased over the years, because they have become a safe and effective alternative to the Vitamin-K antagonists in various clinical scenarios. With their increased use, reports have emerged describing their failure. STUDY QUESTION: What are the patient characteristics and clinical settings in which DOAC treatment failure manifests? DATA SOURCES: We searched published reports in Google Scholar, PubMed, MEDLINE, and Embase from the introduction of DOACs in any therapy until March 2019. STUDY DESIGN: Information on patient characteristics, comorbidities, primary anticoagulation indications, pharmacologic treatment, and outcomes were collected. Primary endpoints were new thrombus formation, failure of resolution of an existing thrombus, or discovery of subtherapeutic drug level. Other endpoints were time to treatment failure, manifestations of treatment failure, and new treatment after DOAC failure. RESULTS: Our search yielded 51 manuscripts, describing 79 patients who exhibited DOAC failure. The most common treatment failures were in patients with antiphospholipid syndrome (44.3%), atrial fibrillation (30.4%), and deep venous thrombosis (6.3%). There was a trend toward higher failure rate for rivaroxaban (65.8%) followed by dabigatran (27.8%), apixaban (7.6%), and then edoxaban (1.3%). Each agent had different median failure times. Most common manifestations of treatment failure were stroke/transient ischemic attack (20.3%), pulmonary embolism (19.0%), and deep venous thrombosis (19.0%). More than half of patients were transitioned to a Vitamin-K antagonist after DOAC failure (55.7%). CONCLUSIONS: Our analysis illustrates that DOACs may fail in the setting of Food and Drug Administration and non-Food and Drug Administration- approved indications. In clinical practice, it may be best to choose between available anticoagulant drugs on a case-by-case basis.

Use of Direct Oral Anticoagulants in the Treatment of Left Ventricular Thrombus: Systematic Review of Current Literature.

BACKGROUND: Left ventricular thrombus (LVT) is an important complication in the setting of systolic dysfunction, particularly after acute myocardial infarction. Current guidelines recommend the vitamin-K antagonist, warfarin, for the treatment of LVT. AREA OF UNCERTAINTY AND STUDY QUESTION: The direct oral anticoagulants (DOACs) are being increasingly used for the management of this entity, despite lack of randomized trials in support of it or knowledge about their efficacy. We aimed to assess the frequency of use and the efficacy of DOACs in the treatment of LVT. DATA SOURCES: We searched published articles in Google Scholar, PubMed, MEDLINE, and Embase from the introduction of DOACs in any therapy until April 2018. Reports describing patients diagnosed with LVT and who were treated with a DOAC were examined. Patient characteristics, comorbidities, pharmacologic treatments, and outcomes were collected. The primary end points of this study were thrombus resolution and time to resolution. Other end points were bleeding and thromboembolic events. RESULTS: Thirty articles describing 41 patients were analyzed. The most common risk factors for LVT formation were male gender, ischemic heart disease, and low ejection fraction. Most patients were treated with rivaroxaban (51.2%), followed by apixaban (26.8%) and dabigatran (22%). Patients were treated with DOAC alone (46.3%), DOAC and aspirin (12.2%), DOAC and clopidogrel (2.4%), and triple therapy (39%). Thrombus resolution success rate was 81%, 100%, and 88.9% for rivaroxaban, apixaban, and dabigatran, respectively. The median time of thrombus resolution was 40 days, 36 days, and 24 days for rivaroxaban, apixaban, and dabigatran, respectively. One nonfatal bleeding event and one stroke event were reported while on a DOAC. CONCLUSIONS: The use of DOACs is a reasonable alternative to vitamin-K antagonists in the management of LVT.

Influence of albuminuria and glomerular filtration rate on blood pressure response to antihypertensive drug therapy.

BACKGROUND: Albuminuria and glomerular filtration rate (GFR), two factors linked to kidney and vascular function, may influence longitudinal blood pressure (BP) responses to complex antihypertensive drug regimens. METHODS: We reviewed the clinic records of 459 patients with hypertension in an urban, academic practice. RESULTS: Mean patient age was 57-years, 89% of patients were African American, and 69% were women. Mean patient systolic/diastolic BP (SBP/DBP) at baseline was 171/98 mmHg while taking an average of 3.3 antihypertensive medications. At baseline, 27% of patients had estimated (e)GFR <60 ml/min/1.73(2), 28% had micro-albuminuria (30-300 mg/g) and 16% had macro-albuminuria (>300 mg/g). The average longitudinal BP decline over the observation period (mean 7.2 visits) was 25/12 mmHg. In adjusted regression models, macro-albuminuria predicted a 10.3 mmHg lesser longitudinal SBP reduction (p < 0.001) and a 7.9 mmHg lesser longitudinal DBP reduction (p < 0.001); similarly eGFR <60 ml/min/1.73(2) predicted an 8.4 mmHg lesser longitudinal SBP reduction (p < 0.001) and a 4.5 lesser longitudinal DBP reduction (p < 0.001). Presence of either micro- or macro-albuminuria, or lower eGFR, also significantly delayed the time to attainment of goal BP. CONCLUSIONS: These data suggest that an attenuated decline in BP in drug-treated hypertensives, resulting in higher average BP levels over the long-term, may mediate a portion of the increased risk of cardiovascular-renal disease linked to elevated urinary albumin excretion and reduced eGFR.

Left ventricular pseudoaneurysm as a fatal complication of purulent pericarditis.

We report a case of a 48-year-old man with purulent pericarditis by Streptococcus viridans, despite aggressive treatment with antibiotics and partial pericardiectomy was complicated by left ventricle pseudo-aneurysm resulting in a fatal outcome. The case highlights the course of complicated purulent pericarditis and the use of noninvasive imaging for assessing early signs of pseudoaneurysm and its typical progression.

Coronary vascular dysfunction in premenopausal women with diabetes mellitus.

BACKGROUND: Diabetes mellitus abolishes the sex differential in coronary artery disease morbidity and mortality in premenopausal women. This finding is independent of other diabetes-associated risk factors, suggesting that other mechanisms such as impaired coronary vascular function may contribute to the increased cardiovascular risk in women with diabetes. The objective of this study was to investigate the effect of diabetes on coronary vascular function in premenopausal women. METHODS: We studied 13 premenopausal women with diabetes (aged 41 +/- 10 years) who were free of overt cardiovascular complications, and 21 control women (12 age-matched and 9 postmenopausal [aged 56 +/- 8 years]). We used [13N]-ammonia as the flow tracer and positron emission testing to measure myocardial blood flow (MBF) at rest, during maximal hyperemia, and in response to cold pressor testing. RESULTS: Baseline MBF was lower in the postmenopausal controls, reflecting the differences in cardiac work and oxygen demand as assessed by the rate-pressure product. However, baseline MBFs were similar in the 3 groups after normalization for differences in the rate-pressure product. During hyperemia, MBF increased and coronary vascular resistance decreased significantly in the 3 groups. However, the increase (from baseline) in MBF in the women with diabetes (164% +/- 58%) was less than in the premenopausal controls (258% +/- 81%, P =.021), but not significantly different from the postmenopausal control women (204% +/- 104%, P =.51). Likewise, the increase in MBF in response to cold pressor testing in the women with diabetes (24% +/- 19%) was significantly lower than in the premenopausal controls (60% +/- 39%, P =.013), but similar to that in postmenopausal control women (27% +/- 15%, P =.97). These differences persisted after adjusting for age and diabetes-associated metabolic abnormalities. CONCLUSIONS: These results demonstrate reduced coronary vasodilator function and impaired response of resistance vessels to increased sympathetic stimulation in premenopausal women with diabetes, similar to those observed in healthy postmenopausal women in whom the sex differential in coronary artery disease morbidity and mortality is no longer present.

Two-dimensional strain profiles in patients with physiological and pathological hypertrophy and preserved left ventricular systolic function: a comparative analyses.

OBJECTIVE: This study was designed to examine the utility of two-dimensional strain (2DS) or speckle tracking imaging to typify functional adaptations of the left ventricle in variant forms of left ventricular hypertrophy (LVH). DESIGN: Cross-sectional study. SETTING: Urban tertiary care academic medical centres. PARTICIPANTS: A total of 129 subjects, 56 with hypertrophic cardiomyopathy (HCM), 34 with hypertensive left ventricular hypertrophy (H-LVH), 27 professional athletes with LVH (AT-LVH) and 12 healthy controls in sinus rhythm with preserved left ventricular systolic function. METHODS: Conventional echocardiographic and tissue Doppler examinations were performed in all study subjects. Bi-dimensional acquisitions were analysed to map longitudinal systolic strain (automated function imaging, AFI, GE Healthcare, Waukesha, Wisconsin, USA) from apical views. RESULTS: Subjects with HCM had significantly lower regional and average global peak longitudinal systolic strain (GLS-avg) compared with controls and other forms of LVH. Strain dispersion index, a measure of regional contractile heterogeneity, was higher in HCM compared with the rest of the groups. On receiver operator characteristics analysis, GLS-avg had excellent discriminatory ability to distinguish HCM from H-LVH area under curve (AUC) (0.893, p<0.001) or AT-LVH AUC (0.920, p<0.001). Tissue Doppler and LV morphological parameters were better suited to differentiate the athlete heart from HCM. CONCLUSIONS: 2DS (AFI) allows rapid characterisation of regional and global systolic function and may have the potential to differentiate HCM from variant forms of LVH.

Predictors of stroke in patients with severe systolic dysfunction in sinus rhythm: role of echocardiography.

BACKGROUND: Congestive heart failure in sinus rhythm ranks second after atrial fibrillation (AF) among cardiogenic risk-factors for stroke. Clinical and echocardiographic predictors of stroke in this high-risk population remain poorly defined. METHODS: Retrospective screening of 1886 consecutive patients with severe systolic dysfunction (LVEF ≤35%) at a tertiary medical center echocardiography database (Nov 2005-Sep 2008) identified 83 patients in sinus rhythm with cardioembolic stroke. Patients with AF on follow-up, prosthetic valve, ventricular arrhythmia and lack of consensus between reviewing neurologists were excluded (n=10). Consecutive age and gender-matched controls in sinus rhythm formed GpII (n=73). RESULTS: The incidence of stroke was 3.9% (73/1886) over 35 months in this study. There were no significant differences in prevalence of established clinical risk-factors for stroke. There was a significantly higher prevalence of LV non-compaction (p=0.02), aneurysm (p<0.01), spontaneous echo-contrast (p<0.01) and pulmonary hypertension (p<0.001) in GpI. CONCLUSIONS: LV non-compaction, aneurysm, spontaneous echo-contrast and pulmonary hypertension are associated with an increased risk of stroke. While anticoagulation of these high-risk subgroups appears reasonable, further study in a prospective randomized clinical trial merits consideration.

WITHDRAWN: Clinical and echocardiographic predictors of cerebrovascular events and left ventricular thrombus in patients with severe systolic dysfunction in sinus rhythm.

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Myocardial injury in thrombotic thrombocytopenic purpura: a frequent, perplexing complication.

BACKGROUND: Although thrombotic thrombocytopenic purpura (TTP) typically involves the heart, angina and myocardial injury are uncommonly reported; fatal cardiogenic shock is exceptional. METHODS: We analyzed 26 patients with TTP who had objective evidence of myocardial injury. RESULTS: Myocardial injury was evident in 6 patients. None had coronary disease. Mean age was 43.6 years; four patients (66%) were female. Mean troponin, creatinine and hemoglobin levels were 7.82 ng/dL (

Cardiac troponin-I: a predictor of prognosis in subarachnoid hemorrhage.

BACKGROUND: Release of cardiac biomarkers is reported in patients with subarachnoid hemorrhage (SAH). Data addressing the impact of cardiac injury on outcome in these patients is sparse. This study was conducted to ascertain the association of elevation of serum cardiac Troponin-I (cTnI) with mortality and neurological outcome in patients with SAH. METHODS: Medical records of all patients admitted with a diagnosis of SAH and at least one measured cTnI were reviewed. Demographic and clinical variables including admission neurological status were collected. Conservative and non-parametric statistics were used to assess association between cTnI and death or neurological outcome at discharge. RESULTS: The study group comprised of 83 patients with a mean age of 59 years. There was a female (60%) and African-American (60%) preponderance. At admission, the median Glasgow Coma Scale (GCS) was 9, and 47% had a severe Hunt-Hess grade (HHG) of > or =4. Elevation of cTnI was found in 31 (37%) patients and was associated with worse baseline Fisher grade (p=0.01) and neurological status: GCS score (p=0.006) and HHG (p=0.007). Patients with abnormal cTnI were more likely to die (55% vs.27%; odds ratio 1.3-8.4, p = 0.01) and had a worse GCS score (p = 0.008) and HHG (p = 0.004) on discharge. On multivariate analysis, peak cTnI (p = 0.04) and admission GCS score of <12 (p = 0.02) were independent predictors of death at discharge. CONCLUSION: Patients with subarachnoid hemorrhage and elevated cTnI are found to have worse neurological status at admission. These patients have a worse neurological outcome and in-hospital mortality.