Creating accountable care for carotid angioplasty and stenting: A multidisciplinary carotid revascularization board.

BACKGROUND: We tested the feasibility of a mandated multidisciplinary carotid revascularization board (MDCB) to review, approve and monitor all carotid artery and stenting (CAS) procedures and outcomes at our institution. METHODS: The board was composed of vascular surgeons, cardiologists, interventional neuroradiologists, neurosurgeons, and neurologists, who met weekly to facilitate an evidence-based, consensus recommendation to ensure appropriate CAS referral. RESULTS: The board successfully reviewed and continues to review and approve all CAS procedures at our center. Of the 69 patients considered high risk for standard surgical treatment, 42 patients were symptomatic and 27 patients were asymptomatic. Their mean age was 70.5-year-old and the median degree of stenosis was 79%. In the 74 procedures, periprocedural complications occurred at the following rates: 2.7% death, 2.7% major stroke, 2.7% minor stroke, and 2.7% myocardial infarction (MI) within 30 days of the procedure. At 1 year the primary endpoints of ipsilateral stroke and neurovascular-related death were observed in 8.1% and 2.7% of the patients, respectively. At mean follow-up of 21 months, 18.8% of the patients (13/69) had died (including all causes), and 14.5% (10/69) experienced stroke (including nontarget strokes). Target vessel revascularization was needed in 2.9% patients. CONCLUSIONS: A mandated multidisciplinary carotid revascularization board MDCB is feasible and potentially advantageous in real clinical practice. It establishes a model for accountable care by providing a mechanism for institutional oversight, credentialing operators, quality review, standardizing care, cost containment and eliminating the "subspecialty silo mentality."

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.

Treatment of heart failure in patients with diabetes mellitus.

Patients with diabetes mellitus have an increased morbidity and mortality from cardiovascular disease. Both coronary artery disease and congestive heart failure (CHF) are largely responsible for the increased cardiovascular adverse events in patients with diabetes. This review discusses the pathophysiology of CHF, the mechanisms of left ventricular (LV) dysfunction and the neurohormonal mechanisms involved in both LV dysfunction and CHF. Diabetes with and without hypertension is an important cause of LV dysfunction and CHF. Diabetes may be responsible for the metabolic and ultrastructural causes of LV dysfunction, while hypertension may be responsible for the marked fibrotic changes that are found. Experimental induction of diabetes in animals has shed light on the biochemical and ultrastructural changes seen. The role of insulin to reverse both metabolic and structural changes is reviewed both from experimental data and with the limited amount of clinical data available. The therapy of CHF in patients with diabetes is similar to that of patients without diabetes, with therapy directed toward the use of beta-blockers and angiotensin converting enzyme (ACE) inhibitors. As the morbidity and mortality are higher in patients with diabetes, several studies have pointed out the importance of this subgroup where the opportunity to make a significant clinical impact exists. A significant opportunity exists to reduce morbidity and mortality with beta-blockers and ACE inhibitors when ischaemia and CHF are both present. However, studies in patients diabetes have been limited to post hoc subgroup analyses and rarely as predefined subgroups. Clinical trials involving patients with diabetes with and without hypertension and LV dysfunction are clearly needed in the future to adequately address the needs of this high risk subgroup.