Research Spotlight

Kopecky, K., A. Afzal, J. Felius, S. A. Hall, J. C. Mendez, M. Assar, D. P. Mason and A. S. Bindra (2017). “Bilateral sympathectomy for treatment of refractory ventricular tachycardia.” Pacing Clin Electrophysiol: 2017 Aug [Epub ahead of print].

Full text of this article.

Ventricular tachycardia (VT) commonly occurs in patients with ischemic or non-ischemic cardiomyopathy and requires anti-arrhythmic drugs, ablation or advanced circulatory support. However, life-threatening VT may be refractory to these therapies, and may cause frequent implantable cardioverter defibrillator (ICD) discharges. Left cardiac sympathetic denervation reduces the occurrence of these fatal arrhythmias by inhibiting the sympathetic outflow to the cardiac tissue. We present a 69-year-old man with non-ischemic cardiomyopathy, life-threatening VT, and hemodynamic instability with numerous ICD discharges who remained refractory to antiarrhythmic drug therapy and ablation attempts. He was effectively treated with bilateral cardiac sympathectomy. Six months later, he remained free of VT with no ICD discharges.

Mueller-Kronast, N. H., O. O. Zaidat, M. T. Froehler, R. Jahan, M. A. Aziz-Sultan, R. P. Klucznik, J. L. Saver, F. R. Hellinger, Jr., D. R. Yavagal, T. L. Yao, D. S. Liebeskind, A. P. Jadhav, R. Gupta, A. E. Hassan, C. O. Martin, H. Bozorgchami, R. Kaushal, R. G. Nogueira, R. H. Gandhi, E. C. Peterson, S. R. Dashti, C. A. Given, 2nd, B. P. Mehta, V. Deshmukh, S. Starkman, I. Linfante, S. H. McPherson, P. Kvamme, T. J. Grobelny, M. S. Hussain, I. Thacker, N. Vora, P. R. Chen, S. J. Monteith, R. D. Ecker, C. M. Schirmer, E. Sauvageau, A. Abou-Chebl, C. P. Derdeyn, L. Maidan, A. Badruddin, A. H. Siddiqui, T. M. Dumont, A. Alhajeri, M. A. Taqi, K. Asi, J. Carpenter, A. Boulos, G. Jindal, A. S. Puri, R. Chitale, E. M. Deshaies, D. H. Robinson, D. F. Kallmes, B. W. Baxter, M. A. Jumaa, P. Sunenshine, A. Majjhoo, J. D. English, S. Suzuki, R. D. Fessler, J. E. Delgado Almandoz, J. C. Martin and D. C. Haussen (2017). “Systematic evaluation of patients treated with neurothrombectomy devices for acute ischemic stroke: Primary results of the stratis registry.” Stroke: 2017 Aug [Epub ahead of print].

Full text of this article.

BACKGROUND AND PURPOSE: Mechanical thrombectomy with stent retrievers has become standard of care for treatment of acute ischemic stroke patients because of large vessel occlusion. The STRATIS registry (Systematic Evaluation of Patients Treated With Neurothrombectomy Devices for Acute Ischemic Stroke) aimed to assess whether similar process timelines, technical, and functional outcomes could be achieved in a large real world cohort as in the randomized trials. METHODS: STRATIS was designed to prospectively enroll patients treated in the United States with a Solitaire Revascularization Device and Mindframe Capture Low Profile Revascularization Device within 8 hours from symptom onset. The STRATIS cohort was compared with the interventional cohort of a previously published SEER patient-level meta-analysis. RESULTS: A total of 984 patients treated at 55 sites were analyzed. The mean National Institutes of Health Stroke Scale score was 17.3. Intravenous tissue-type plasminogen activator was administered in 64.0%. The median time from onset to arrival in the enrolling hospital, door to puncture, and puncture to reperfusion were 138, 72, and 36 minutes, respectively. The Core lab-adjudicated modified Thrombolysis in Cerebral Infarction >/=2b was achieved in 87.9% of patients. At 90 days, 56.5% achieved a modified Rankin Scale score of 0 to 2, all-cause mortality was 14.4%, and 1.4% suffered a symptomatic intracranial hemorrhage. The median time from emergency medical services scene arrival to puncture was 152 minutes, and each hour delay in this interval was associated with a 5.5% absolute decline in the likelihood of achieving modified Rankin Scale score 0 to 2. CONCLUSIONS: This largest-to-date Solitaire registry documents that the results of the randomized trials can be reproduced in the community. The decrease of clinical benefit over time warrants optimization of the system of care.

Khanna, A., S. W. English, X. S. Wang, K. Ham, J. Tumlin, H. Szerlip, L. W. Busse, L. Altaweel, T. E. Albertson, C. Mackey, M. T. McCurdy, D. W. Boldt, S. Chock, P. J. Young, K. Krell, R. G. Wunderink, M. Ostermann, R. Murugan, M. N. Gong, R. Panwar, J. Hastbacka, R. Favory, B. Venkatesh, B. T. Thompson, R. Bellomo, J. Jensen, S. Kroll, L. S. Chawla, G. F. Tidmarsh and A. M. Deane (2017). “Angiotensin ii for the treatment of vasodilatory shock.” N Engl J Med 377(5): 419-430.

Full text of this article.

BACKGROUND: Vasodilatory shock that does not respond to high-dose vasopressors is associated with high mortality. We investigated the effectiveness of angiotensin II for the treatment of patients with this condition. METHODS: We randomly assigned patients with vasodilatory shock who were receiving more than 0.2 mug of norepinephrine per kilogram of body weight per minute or the equivalent dose of another vasopressor to receive infusions of either angiotensin II or placebo. The primary end point was a response with respect to mean arterial pressure at hour 3 after the start of infusion, with response defined as an increase from baseline of at least 10 mm Hg or an increase to at least 75 mm Hg, without an increase in the dose of background vasopressors. RESULTS: A total of 344 patients were assigned to one of the two regimens; 321 received a study intervention (163 received angiotensin II, and 158 received placebo) and were included in the analysis. The primary end point was reached by more patients in the angiotensin II group (114 of 163 patients, 69.9%) than in the placebo group (37 of 158 patients, 23.4%) (odds ratio, 7.95; 95% confidence interval [CI], 4.76 to 13.3; P<0.001). At 48 hours, the mean improvement in the cardiovascular Sequential Organ Failure Assessment (SOFA) score (scores range from 0 to 4, with higher scores indicating more severe dysfunction) was greater in the angiotensin II group than in the placebo group (-1.75 vs. -1.28, P=0.01). Serious adverse events were reported in 60.7% of the patients in the angiotensin II group and in 67.1% in the placebo group. Death by day 28 occurred in 75 of 163 patients (46%) in the angiotensin II group and in 85 of 158 patients (54%) in the placebo group (hazard ratio, 0.78; 95% CI, 0.57 to 1.07; P=0.12). CONCLUSIONS: Angiotensin II effectively increased blood pressure in patients with vasodilatory shock that did not respond to high doses of conventional vasopressors.

Packer, M., S. D. Anker, J. Butler, G. Filippatos and F. Zannad (2017). “Effects of sodium-glucose cotransporter 2 inhibitors for the treatment of patients with heart failure: Proposal of a novel mechanism of action.” JAMA Cardiol: 2017 Aug [Epub ahead of print].

Full text of this article.

Importance: Only 1 class of glucose-lowering agents-sodium-glucose cotransporter 2 (SGLT2) inhibitors-has been reported to decrease the risk of cardiovascular events primarily by reducing the risk of the development or progression of heart failure. In a landmark trial called Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes [EMPA-REG Outcomes], long-term treatment with empagliflozin prevented fatal and nonfatal heart failure events but did not reduce the risk of myocardial infarction or stroke in diabetic patients. Observations: The beneficial effect of SGLT2 inhibitors on heart failure cannot be explained by their actions on glycemic control or as osmotic diuretics. Instead, in the kidneys, SGLT2 functionally interacts with the sodium-hydrogen exchanger, which is responsible for the majority of sodium tubular reuptake following filtration. The activity of sodium-hydrogen exchanger is markedly increased in patients with heart failure and may be responsible for both resistance to diuretics and to endogenous natriuretic peptides. In addition, in the heart, empagliflozin appears to inhibit sodium-hydrogen exchange, which may in turn lead to a reduction in cardiac injury, hypertrophy, fibrosis, remodeling, and systolic dysfunction. Furthermore, the major pathophysiological derangements of heart failure and a preserved ejection fraction may be mitigated by the actions of SGLT2 inhibitors to reduce blood pressure, body weight, and fluid retention as well as to improve renal function. The benefits of spironolactone in patients with heart failure with either a reduced or a preserved ejection fraction may also be attributable to the actions of the drug to inhibit the sodium-hydrogen exchange mechanism. Conclusions and Relevance: The benefits of SGLT2 inhibitors in heart failure may be mediated by the inhibition of sodium-hydrogen exchange rather than the effect on glucose reabsorption. This hypothesis has important implications for the design and analysis of large-scale outcomes trials involving diabetic or nondiabetic patients with chronic heart failure.

Cedars, A., L. Benjamin, S. V. Burns, E. Novak and A. Amin (2017). “Clinical predictors of length of stay in adults with congenital heart disease.” Heart 103(16): 1258-1263.

Full text of this article.

OBJECTIVE: Length of stay (LOS) is a major driver of inpatient care costs. To date, few studies have investigated risk factors associated with increased LOS in patients with adult congenital heart disease (ACHD). In the present work, we sought to address this knowledge gap. METHODS: We conducted an analysis of the State Inpatient Databases from Arkansas, California, Florida, Hawaii, Nebraska and New York. We analysed data on admissions in patients with ACHD and constructed a series of hierarchical regression models to identify the clinical factors having the greatest effects on LOS. RESULTS: We identified 99 103 inpatient hospitalisations meeting criteria for inclusion. Diagnoses associated with the longest LOS were septicaemia (LOS=14.2 days in patients atrial septal defect, and 11.7 days among all other ACHD) and pericarditis, endocarditis and myocarditis (LOS=13.6 days and 10.0 days, respectively). When separated by underlying anatomy, the variables most consistently associated with longer LOS were bacterial infection, complications of surgeries or medical care, acute renal disease and anaemia. CONCLUSIONS: In the present study, we identified risk factors associated with longer LOS in ACHD. These data may be used to identify at-risk patients for targeted intervention to decrease LOS and thereby cost.