Rishi Sukhija

Effect of Statins on Fasting Plasma Glucose in Diabetic and Nondiabetic Patients

Background The 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) reduce serum cholesterol level and cardiovascular morbidity and mortality. However, the effect of statins on glucose metabolism is unclear. Some studies have suggested that statins may cause hyperglycemia by increasing calcium concentration in the islet cells leading to decrease in insulin release or by decreasing GLUT 4-mediated peripheral glucose uptake. Methods We analyzed the data in 345,417 patients (mean age 61 ± 15 years, 94% males, 6% diabetic, 20% statin users) from the Veterans Affairs VISN 16 database. We studied change in fasting plasma glucose (FPG) in this population over a mean time of 2 years between the first available measurement and the last measurement form the most recent recorded visit. Data were limited to patients who had 2 FPG measurements. Diagnosis of diabetes had to be present before the first FPG measurement. Results Among patients without diabetes, FPG increased with statin use from 98 mg/dL to 105 mg/dL, and among nonstatin users, FPG increased from 97 mg/dL to 101 mg/dL (increase in FPG with statin use P < 0.0001). Among patients with diabetes, FPG increased with statin use from 102 mg/dL to 141 mg/dL, and among nonstatin users, FPG increased from 100 mg/dL to 129 mg/dL (increase in FPG with statin use; P < 0.0001). After adjustment for age and use of aspirin, β-blockers, and angiotensin-converting enzyme inhibitors, the change in FPG in nondiabetic statin users was 7 mg/dL (vs 5 mg/dL in nonstatin users, P < 0.0001) and for diabetic statin users it was 39 mg/dL (vs 32 in nonstatin users, P < 0.0001). Conclusions Statin use is associated with a rise of FPG in patients with and without diabetes. This relationship between statin use and rise in FPG is independent of age and use of aspirin, β-blockers, and angiotensin-converting enzyme inhibitors.

Relation of Cardiac Troponin I Levels With In-Hospital Mortality in Patients With Ischemic Stroke, Intracerebral Hemorrhage, and Subarachnoid Hemorrhage

Troponin I levels were drawn within 24 hours of stroke in 161 of 175 patients (92%) with ischemic stroke, 94 of 107 patients (88%) with intracerebral hemorrhage, and 96 of 96 patients (100%) with subarachnoid hemorrhage. A troponin level >0.4 ng/ml was considered increased. In patients with ischemic stroke, in-hospital mortality occurred in 15 of 23 patients (65%) with increased troponin I compared with 6 of 138 patients (4%) with normal troponin I (p <0.001). In patients with intracerebral hemorrhage, in-hospital mortality occurred in 9 of 14 patients (64%) with increased troponin I compared with 22 of 80 patients (28%) with normal troponin I (p <0.005). In patients with subarachnoid hemorrhage, in-hospital mortality occurred in 8 of 20 patients (40%) with increased troponin I compared with 8 of 76 patients (11%) with normal troponin I (p <0.005). In conclusion, patients with ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage with elevated troponin I levels have increased in-hospital mortality.

Common carotid artery wall thickness and external diameter as predictors of prevalent and incident cardiac events in a large population study

BackgroundArterial diameters enlarge in response to wall thickening, plaques, and many atherosclerotic risk factors. We hypothesized that right common carotid artery (RCCA) diameter would be independently associated with cardiac disease and improve risk discrimination.MethodsIn a middle-aged, biracial population (baseline n = 11225), we examined associations between 1 standard deviation increments of baseline RCCA diameter with prevalent myocardial infarction (MI) and incident cardiac events (MI or cardiac death) using logistic regression and Cox proportional hazards models, respectively. Areas under the receiver operator characteristic curve (AUC) were used to estimate model discrimination.ResultsMI was present in 451 (4%) participants at baseline (1987–89), and incident cardiac events occurred among 646 (6%) others through 1999. Adjusting for IMT, RCCA diameter was associated with prevalent MI (female OR = 2.0, 95%CI = 1.61–2.49; male OR = 1.16, 95% CI = 1.04–1.30) and incident cardiac events (female HR = 1.75, 95% CI = 1.51–2.02; male HR = 1.27, 95% CI = 1.15–1.40). Associations were attenuated but persisted after adjustment for risk factors (not including IMT) (prevalent MI: female OR = 1.73, 95% CI = 1.40–2.14; male OR = 1.14, 95% CI = 1.02–1.28, and incident cardiac events: female HR = 1.26, 95% CI = 1.08–1.48; male HR = 1.19, 95% CI = 1.08–1.32). After additional adjustment for IMT, diameter was associated with incident cardiac events in women (HR = 1.18, 95% CI = 1.00–1.40) and men (HR = 1.17, 95% CI = 1.06–1.29), and with prevalent MI only in women (OR = 1.73; 95% CI = 1.37–2.17). In women, when adjustment was limited, diameter models had larger AUC than other models.ConclusionRCCA diameter is an important correlate of cardiac events, independent of IMT, but adds little to overall risk discrimination after risk factor adjustment.

Percutaneous intervention on the saphenous vein bypass grafts--long-term outcomes.

Background/Objective: In this era of drug eluting stents (DES), the long‐term outcome of percutaneous intervention (PCI) on saphenous venous grafts (SVG) is unknown. The objective of the study was to compare the long‐term outcomes of DES versus bare metal stent (BMS) in this population and to determine the predictors of outcomes. Methods: We reviewed the medical records of all patients who had PCI performed during January 2003 to February 2005 to obtain data cardiac risk factors, medications at discharge, angiographic details and outcomes. Results: One hundred and nine patient had PCI to SVG; of these, 37 patients received DES and the remaining had BMS. Over a mean follow‐up of 33 months, the PCI using DES was associated with 30% restenosis, 35% target vessel revascularization (TVR) and major adverse cardiac event (MACE) rate of 46% versus 35% restenosis, 38% TVR and 50% MACE rate with BMS. There was no significant difference in long‐term outcome with DES as compared to BMS. Conclusion: There was no difference in the long‐term outcomes of PCI on SVG irrespective of the type of stent used.

Effect of statins on the development of renal dysfunction.

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) decrease serum cholesterol. Dyslipidemia is believed to be associated with the development of renal dysfunction. It was postulated that statins may reduce the development of renal dysfunction. The effect of statin use on the development of renal dysfunction in 197,551 patients (Department of Veterans Affairs, Veterans Integrated Service Network 16 [VISN16] database) was examined. Of these patients, 29.5% (58,332 patients) were statin users and 70.5% (139,219 patients) were not. Development of renal dysfunction was defined as doubling of baseline creatinine or increase in serum creatinine > or =0.5 mg/dl from the first to last measurement with a minimum of 90 days in between. During 3.1 years of follow-up, 3.4% of patients developed renal dysfunction. After adjustment for demographics, diabetes mellitus, smoking, hypertension, and other medications (mainly angiotensin-converting enzyme inhibitors, calcium channel blockers, and aspirin), use of statins decreased the odds of developing renal dysfunction by 13% (odds ratio [OR] 0.87, 95% confidence interval [CI] 0.82 to 0.92, p <0.0001). The beneficial effect of statins appeared to be independent of the decrease in cholesterol. Other variables that affected the development of renal dysfunction were age (OR 1.04, 95% CI 1.03 to 1.04, p <0.0001), diabetes (OR 1.77, 95% CI 1.68 to 1.86, p <0.0001), hypertension (OR 1.11, 95% CI 1.02 to 1.2, p = 0.0153), and smoking (OR 1.12, 95% CI 1.02 to 1.24, p = 0.0244). In conclusion, statin use may retard the development of renal dysfunction. The beneficial effect of statins in preventing the development of renal dysfunction appears to be independent of their lipid-lowering effect.

Mortality, left ventricular ejection fraction, and prevalence of new left ventricular wall motion abnormality at long-term follow-up in patients with implantable cardioverter defibrillators treated with biventricular pacing versus right ventricular pacing.

We investigated left ventricular ejection fraction and new left ventricular wall motion abnormality before pacemaker implantation and at follow-up and mortality at long-term follow-up in 81 patients with implantable cardioverter defibrillators treated with biventricular pacing and in 80 patients with implantable cardioverter defibrillators treated with DDDR-70 right ventricular pacing. At 23-month follow-up, the left ventricular ejection fraction decreased from 36% to 30% in patients treated with right ventricular pacing and increased at 38-month follow-up from 35% to 40% in patients treated with biventricular pacing (P < 0.001). New left ventricular wall motion abnormality developed at 23-month follow-up in 23 of 80 patients (29%) treated with right ventricular pacing and at 38-month follow-up in 7 of 81 patients (9%) treated with biventricular pacing (P < 0.005). Tweny-two of 80 patients (28%) treated with right ventricular pacing died at 45-month follow-up and 8 of 81 patients (10%) treated with biventricular pacing died at 53-month follow-up (P < 0.01).

Systolic compression of left main coronary artery by left ventricular pseudoaneurysm complicated by critical stenosis of left main coronary artery

A 69-year-old man was admitted to the hospital with complaints of exertional substernal chest pain and dyspnea for 3 weeks. His medical history consisted of dyslipidemia, type 2 diabetes mellitus, and valvular heart disease. He had a mitral commissurotomy through a left thoracotomy for mitral stenosis at age 16 years followed by mitral valve replacement with a 25 mm Carpentier Edwards bovine pericardial prosthesis in February, 2007. He also had a aortic valve replacement with a 19 mm Carpentier Edwards bovine pericardial prosthesis at that time. On this admission, he had a maximum troponin I level of 0.12 (normal < 0.05 ng/ml), a creatine kinase-MB fraction of 3.4 (normal < 5.0 ng/ml), and a creatine phosphokinase of 288 (normal 35-232 U/l). Coronary angiography revealed near complete systolic obliteration of the left main coronary artery with normal caliber in diastole and discrete stenosis of the mid left anterior descending coronary artery resulting in 40% obstruction of the vessel (Figure 1A). Left ventriculography revealed systolic aneurysmal dilatation of a segment of the left ventricle (LV) compressing the left main coronary artery in systole and a LV ejection fraction of 50% (Figure 1B). Figure 1 Findings on the initial cardiac catheterization. A – Baseline coronary angiogram in left anterior oblique caudal view demonstrating systolic compression of the left main coronary artery (LM). B – Left anterior oblique cranial view of initial ... A thoracic computed tomography (CT) scan and a transesophageal echocardiogram (TEE) were obtained to provide anatomical delineation of the LV pseudoaneurysm The thoracic CT scan revealed an abnormal 3 cm × 2.4 cm contrast-filled structure to the left of the aorta, superior to the LV outflow tract, and inferior to the left main coronary artery likely representing a LV pseudoaneurysm. The TEE showed a normal LV ejection fraction, a small inferoposterior wall hypokinesis, and a LV pseudoaneurysm with a 1.3 cm opening originating below the mitral annulus anteriorly adjacent to the left atrial appendage extending superiorly to the left main coronary artery. The patient subsequently had a bovine patch repair of the LV pseudoaneurysm with resection of the left atrial appendage. A coronary angiogram obtained after surgery demonstrated a discrete fixed stenosis of the mid left main coronary artery resulting in 70% obstruction of the vessel (Figure 2). Intravascular ultrasound of the left main coronary artery stenosis revealed a cross sectional area of 2.9 mm2. Figure 2 Coronary angiogram in right anterior oblique caudal view of LM after resection of LV pseudoaneurysm showing evidence of critical LM stenosis The left main coronary artery was predilated with a 3.5 mm × 9 mm balloon inflated to 8 atm for 6 s. The stenosis was treated with a 4.0 mm × 12 mm everlimus drug-eluting stent that was deployed at 8 atm for 12 s with excellent results (Figures 3 and ​and4).4). Intravascular ultrasound imaging after percutaneous coronary intervention revealed a well apposed stent. Figure 3 Coronary angiogram displaying deployment of 4.0 mm × 12 mm PROMOS stent to the LM on right anterior oblique caudal view Figure 4 Right anterior oblique cranial view of LM after deployment of 4.0 mm × 12 mm PROMOS stent. after percutaneous coronary intervention (post PCI) A LV pseudoaneurysm is an incomplete rupture of the LV myocardium that is contained by organized LV thrombus, adherent scar tissue, and portions of the epicardum and parietal pericardium. In comparison to a true LV aneurysm, the LV pseudoaneurysm has a maximal neck to internal orifice width ratio of ≤ 0.5, a saccular or globular chamber, and a turbulent Doppler flow pattern through the neck [1]. The LV pseudoaneurysm can drain off significant portions of each LV stroke volume. A LV pseudoaneurysm can develop due to transmural myocardial infarction, previous ventriculotomy, replacement of the mitral valve, trauma, or infective endocarditis. It occurs in 0.02% to 2.0% of mitral valve replacement surgeries. Factors predisposing to LV psudoaneurysm include resection of the posterior leaflet of the mitral valve, excessive decalcification of the mitral annulus, placement of an oversized mitral valve prosthesis, and reoperation for mitral valve replacement [2]. The LV pseudoaneurysm following mitral valve replacement tends to be subannular in location [3]. Congestive heart failure, chest pain, and dyspnea are the most frequently reported symptoms associated with LV pseudoaneurysm. Approximately 70% of patients have systolic heart murmurs. A pansystolic murmur due to leaking of blood into the LV pseudoaneurysm may be heard on auscultation [4]. The majority of patients have electrocardiographic abnormalities which are usually nonspecific ST-segment changes. Lethal complications of LV pseudoaneurysm are LV failure, LV thrombus formation, embolization, rupture of the aneurysm and death [5]. To the best of our knowledge, there is only one published case of a patient with a history of open mitral commissurotomy and annuloplasty, aortic valve and mitral valve replacement presenting with chest pain and dyspnea with subsequent development of a LV pseudoaneurysm causing systolic compression of the left main coronary artery [6]. Unique to our case was critical left main coronary artery stenosis seen on coronary angiography after surgery which was successfully treated with percutaneous coronary intervention.

Pulmonary hypertension in left heart disease

Corresponding author: Prof. Wilbert S. Aronow MD, FACC Division of Cardiology New York Medical College Macy Pavilion, Room 141 Valhalla, NY10595 USA Phone: 914-493-5311 E-mail: wsaronow@aol.com 1 Department of Cardiology, Maulana Azad Medical College and G.B. Pant Institute of Postgraduate Medical Education and Research, New Delhi, India 2Division of Cardiology, Indiana University La Porte Hospital, La Porte, Indiana, USA 3Division of Cardiology, Indiana University Health, Indianapolis, Indiana, USA 4Division of Cardiology, New York Medical College, Valhalla, NY, USA

199 HYPERGLYCEMIA PREDICTS FAILURE IN PERCUTANEOUS INTERVENTION OF CORONARY CHRONIC TOTAL OCCLUSION.

Objective Hyperglycemia is known to be associated with increased morbidity and mortality in critically ill hospitalized patients. Although the presence of diabetes mellitus is associated with poor outcomes, we sought to determine the effect of periprocedural hyperglycemia on the success of percutaneous intervention (PCI) in coronary chronic total occlusions (CTO). Methods The study cohort included patients undergoing PCI to open CTO and symptoms of > 1 year9s duration. Fasting blood glucose levels were measured on the morning of the procedure day. Postprocedure success, contrast volume, and creatinine elevations were also recorded. Clinical events (death, myocardial infarction, repeat revascularization, and hospitalization for cardiac reasons) over 5 to 12 months of follow-up were recorded. Results Seventy-two patients, all men, mean age 64 ± 9 years, formed the study cohort. PCI was successful in 34 of 72 (47%) patients. Mean follow-up duration was 6 ± 2 months. Periprocedural glucose level was not a significant predictor for major cardiovascular adverse events (MACE) or a rise in creatinine (multivariate analysis controlling for contrast volume). However, fasting blood glucose was significantly lower in group with successful PCI (128 ± 36 vs 171 ± 52 mg/dL, p = .008). In multivariate analysis after controlling for presence of diabetes, contrast volume, and age, periprocedural hyperglycemia remained the only significant independent predictor of PCI outcome. Conclusions Periprocedural hyperglycemia is a powerful predictor of outcome for PCI in CTO of coronary arteries. Aggressive preprocedure glycemic control is likely to improve immediate success in opening CTOs.

PREDICTORS OF IN-STENT RESTENOSIS AND PATIENT OUTCOME AFTER PERCUTANEOUS CORONARY INTERVENTION IN DIABETES MELLITUS.: 77

Background Diabetics have a significantly higher incidence of major adverse cardiac events (MACE) and in-stent restenosis (ISR) than nondiabetics after percutaneous coronary intervention (PCI). Predictors of MACE and ISR are uncertain in diabetics. There are few data about the association of microalbuminuria and diabetic retinopathy with MACE and ISR. Methods We studied 195 patients (63 ± 9 years, 98% males) with diabetes mellitus who underwent PCI. We investigated ISR and incidence of MACE (cumulative of myocardial infarction, revascularization, and deaths from cardiac causes) in these patients; all patients were on statins. Results Of 195 patients, 107 had follow-up catheterization at a mean of 16 months. Of these 107 patients, 56 developed ISR. In the multivariate model, microalbuminuria or diabetic retinopathy did not have any significant association with ISR (OR = 0.659, CI 0.247-1.75, p = .40 and OR = 2.02, CI 0.64-6.37, p = .22, respectively) or MACE (OR = 1.342, CI 0.7-2.55, p = .37 and OR = 0.945, CI 0.437-2.04, p = .88, respectively). Plasma level of HDL cholesterol was inversely associated with the incidence of ISR (OR −0.928, CI 0.876-0.983, p = .011) and MACE (OR −0.965, CI 0.931-1, p = .048). Use of a Cypher stent (vs bare metal stent) had a negative association with ISR (OR −0.171, CI 0.05-0.585, p = .004). The presence of renal disease was associated with higher MACE (OR 3.19, CI 1.45-7.031, p = .0039). The multivariate model was adjusted for the size of the target vessel, complexity of lesion, type of stent, and plasma LDL levels. Conclusion HDL cholesterol level is inversely associated with ISR and MACE after PCI in high-risk diabetic patients. However, microalbuminuria or diabetic retinopathy are not associated with ISR or MACE.