Rahul Sakhuja

Nonculprit plaques in patients with acute coronary syndromes have more vulnerable features compared with those with non-acute coronary syndromes: a 3-vessel optical coherence tomography study.

Background— Patients with acute coronary syndrome (ACS) have a higher incidence of recurrent ischemic events. The aim of this study was to compare the plaque characteristics of nonculprit lesions between ACS and non-ACS patients using optical coherence tomography (OCT) imaging. Methods and Results— Patients who had 3-vessel OCT imaging were selected from the Massachusetts General Hospital (MGH) OCT Registry. MGH registry is a multicenter registry of patients undergoing OCT. The prevalence and characteristics of nonculprit plaques were compared between ACS and non-ACS patients. A total of 248 nonculprit plaques were found in 104 patients: 45 plaques in 17 ACS patients and 203 plaques in 87 non-ACS patients. Compared with plaques of non-ACS patients, plaques of ACS patients had a wider lipid arc (147.3 ± 29.5° versus 116.2 ± 33.7°, P<0.001), a longer lipid length (10.7 ± 5.9 mm versus 7.0 ± 3.7 mm, P=0.002), a larger lipid volume index [averaged lipid arc×lipid length] (1605.5 ± 1013.1 versus 853.4 ± 570.8, P<0.001), and a thinner fibrous cap (70.2 ± 20.2 µm versus 103.3 ± 46.8 µm, P<0.001). Moreover, thin-cap fibroatheroma (64.7% versus 14.9%, P<0.001), macrophage (82.4% versus 37.9%, P=0.001), and thrombus (29.4% versus 1.1%, P<0.001) were more frequent in ACS patients. Although the prevalence of microchannel did not differ between the groups, the closest distance from the lumen to microchannel was shorter in ACS subjects than in non-ACS (104.6 ± 67.0 µm versus 198.3 ± 133.0 µm, P=0.027). Conclusions— Nonculprit lesions in patients with ACS have more vulnerable plaque characteristics compared with those with non-ACS. Neovascularization was more frequently located close to the lumen in patients with ACS.

Non-Culprit Plaques in Patients with Acute Coronary Syndromes (ACS) Have More Vulnerable Features Compared to Those with Non-ACS: A 3-Vessel Optical Coherence Tomography Study

Background— Patients with acute coronary syndrome (ACS) have a higher incidence of recurrent ischemic events. The aim of this study was to compare the plaque characteristics of nonculprit lesions between ACS and non-ACS patients using optical coherence tomography (OCT) imaging. Methods and Results— Patients who had 3-vessel OCT imaging were selected from the Massachusetts General Hospital (MGH) OCT Registry. MGH registry is a multicenter registry of patients undergoing OCT. The prevalence and characteristics of nonculprit plaques were compared between ACS and non-ACS patients. A total of 248 nonculprit plaques were found in 104 patients: 45 plaques in 17 ACS patients and 203 plaques in 87 non-ACS patients. Compared with plaques of non-ACS patients, plaques of ACS patients had a wider lipid arc (147.3 ± 29.5° versus 116.2 ± 33.7°, P<0.001), a longer lipid length (10.7 ± 5.9 mm versus 7.0 ± 3.7 mm, P=0.002), a larger lipid volume index [averaged lipid arc×lipid length] (1605.5 ± 1013.1 versus 853.4 ± 570.8, P<0.001), and a thinner fibrous cap (70.2 ± 20.2 µm versus 103.3 ± 46.8 µm, P<0.001). Moreover, thin-cap fibroatheroma (64.7% versus 14.9%, P<0.001), macrophage (82.4% versus 37.9%, P=0.001), and thrombus (29.4% versus 1.1%, P<0.001) were more frequent in ACS patients. Although the prevalence of microchannel did not differ between the groups, the closest distance from the lumen to microchannel was shorter in ACS subjects than in non-ACS (104.6 ± 67.0 µm versus 198.3 ± 133.0 µm, P=0.027). Conclusions— Nonculprit lesions in patients with ACS have more vulnerable plaque characteristics compared with those with non-ACS. Neovascularization was more frequently located close to the lumen in patients with ACS.

Meta-Analysis of Mortality in Dialysis Patients With an Implantable Cardioverter Defibrillator†

Patients receiving dialysis are at high risk for sudden cardiac death. Although clinical trials have shown that implantable cardioverter-defibrillators (ICDs) are effective in improving survival in a variety of populations, dialysis patients have been routinely excluded from these analyses. The purpose of this meta-analysis was to synthesize the available evidence regarding the effectiveness of ICD therapy in patients receiving dialysis. Medline, EMBASE, Web of Science, and Google Scholar were searched for pertinent studies published from 1999 to 2008. In addition, hand searches of the relevant annual scientific sessions and major scientific meetings in North America and Europe from 2000 to 2008 were performed. All clinical reports describing outcomes of ICD therapy in relation to renal function were eligible. Four investigators independently extracted the data in a standardized manner. Seven studies were identified, with a total of 2,516 patients and 89 patients receiving dialysis. Despite having ICDs, patients receiving dialysis had a 2.7-fold higher mortality compared with those not receiving dialysis. The results were similar in fixed- and random-effects models. Comparing patients receiving dialysis and those with chronic kidney disease but not receiving dialysis, there was no significant difference in mortality (risk ratio 1.62, 95% confidence interval 0.84 to 3.14). No evidence of publication bias was found. In conclusion, this meta-analysis suggests that even in those with ICDs, there is still a 2.7-fold increased mortality risk in patients who receive dialysis compared with those who do not. Beta blockers may be less cardioprotective in patients with ICDs who are on dialysis.

Comparison of incidence and time course of neoatherosclerosis between bare metal stents and drug-eluting stents using optical coherence tomography.

Recent studies have reported the development of neoatherosclerosis inside stents and subsequent acute coronary syndrome secondary to disruption of neointimal hyperplasia. The aim of the study was to compare the characteristics of neointimal hyperplasia and its time course between bare metal stents (BMSs) and drug-eluting stents (DESs) using optical coherence tomography. A total of 138 stents were divided into 3 groups according to the follow-up period: early phase, <9 months (25 BMSs and 27 DESs); intermediate phase, ≥9 and <48 months (18 BMSs and 43 DESs); and delayed phase, ≥48 months (13 BMSs and 12 DESs). Optical coherence tomographic analysis included the presence of lipid-laden intima, percentage of lipid-rich plaque, and signal attenuation. The optical coherence tomographic findings were compared between the BMSs and DESs in each period, and the difference between the periods was also determined. In the early phase, a greater incidence of lipid-laden plaque (37% vs 8%, p = 0.02) and a greater percentage of lipid-rich plaque (12.9 ± 25.1% vs 1.2 ± 4.3%, p = 0.01) were found in the DESs than in the BMSs. In the intermediate phase, the DES group continuously showed a significantly greater incidence of lipid-laden plaque (63% vs 28%, p = 0.03) and greater percentage of lipid-rich plaque (24.8 ± 28.1% vs 4.1 ± 7.3%, p <0.01). In addition, signal attenuation was greater in the DES group, suggesting early changes in neointimal hyperplasia properties. In the delayed phase, lipid-laden plaque was the predominant type in both groups. In conclusion, lipid-rich neoatherosclerosis develops inside stents earlier in DESs than in BMSs. After 48 months, most restenotic stents will have developed lipid-laden neointima in both groups.

Balloon aortic valvuloplasty in the era of transcatheter aortic valve replacement: acute and long-term outcomes.

BACKGROUND The use of balloon aortic valvuloplasty (BAV) has resurged since the development of transcatheter aortic valve replacement (TAVR). The aim of our study was to determine the procedural and long-term outcomes of patients treated by BAV in the early TAVR era. METHODS From 2005 to 2008, 323 consecutive patients presenting with severe aortic stenosis were treated by BAV in our institution. RESULTS Mean age and logistic EuroSCORE were 80.5 ± 9.9 years and 28.7% ± 12.5%, respectively. The effective orifice area increased from 0.68 ± 0.25 to 1.12 ± 0.39 cm(2) (P < .001) after BAV. Inhospital major complications occurred in 22 patients (6.8%), with a mortality rate of 2.5%. Eighty-five patients (26.3%) were bridged to surgical aortic valve replacement (SAVR, 9.6%) or TAVR (16.7%). Twenty-eight patients (8.7%) had at least 1 repeat BAV. Two hundred ten patients (65%) received only medical therapy post-BAV. Mean duration of follow-up was 20.7 ± 20.0 months. Kaplan-Meier analysis demonstrated that survival after single BAV was poor. Patients treated by BAV followed by SAVR or TAVR had the highest long-term survival rate (P < .001). Multivariable analysis revealed that logistic EuroSCORE, severe aortic regurgitation and stroke complications post-BAV, and medical therapy post-BAV were independent predictors of mortality. CONCLUSIONS The results of our study suggest that BAV is an acceptable bridge to SAVR or TAVR in a very high-risk population not immediately suitable for definitive therapy. Balloon aortic valvuloplasty remains only a brief temporizing procedure with a poor long-term outcome without subsequent definitive therapy.

Comparison of nonculprit coronary plaque characteristics between patients with and without diabetes: a 3-vessel optical coherence tomography study.

OBJECTIVES The aim of the present study was to compare the characteristics of nonculprit coronary plaques between diabetes mellitus (DM) and non-DM patients using 3-vessel optical coherence tomography (OCT) imaging. BACKGROUND DM patients have a higher recurrent cardiovascular event rate. METHODS Patients who had undergone 3-vessel OCT imaging were identified from the Massachusetts General Hospital OCT Registry. Characteristics of nonculprit plaques were compared between DM and non-DM patients. RESULTS A total of 230 nonculprit plaques were identified in 98 patients. Compared with non-DM patients, DM patients had a larger lipid index (LI) (averaged lipid arc × lipid length; 778.6 ± 596.1 vs. 1358.3 ± 939.2, p < 0.001) and higher prevalence of calcification (48.4% vs. 72.2%, p = 0.034) and thrombus (0% vs. 8.3%, p = 0.047). DM patients were divided into 2 groups based on glycated hemoglobin (A(1C)) levels of ≤7.9% and ≥8.0%. LI was significantly correlated with diabetic status (778.6 ± 596.1 [non-DM] vs. 1,171.5 ± 708.1 [A(1C) ≤7.9%] vs. 1,638.5 ± 1,173.8 [A(1C) ≥8%], p value for linear trend = 0.005), and fibrous cap thickness was inversely correlated with the A(1C) level (99.4 ± 46.7 μm [non-DM] vs. 91.7 ± 29.6 μm [A(1C) ≤7.9%] vs. 72.9 ± 22.7 μm [A(1C) ≥8%], p value for linear trend = 0.014). Patients with A(1C) ≥8% also had the highest prevalence of thin-cap fibroatheroma (TCFA) and macrophage infiltration. CONCLUSIONS Compared with non-DM patients, DM patients have a larger LI and a higher prevalence of calcification and thrombus. The LI was larger and TCFA and macrophage infiltration were frequent in patients with A(1C) ≥8%.

A Prediction Model to Identify Patients at High Risk for 30-Day Readmission After Percutaneous Coronary Intervention

Background—The Affordable Care Act creates financial incentives for hospitals to minimize readmissions shortly after discharge for several conditions, with percutaneous coronary intervention (PCI) to be a target in 2015. We aimed to develop and validate prediction models to assist clinicians and hospitals in identifying patients at highest risk for 30-day readmission after PCI. Methods and Results—We identified all readmissions within 30 days of discharge after PCI in nonfederal hospitals in Massachusetts between October 1, 2005, and September 30, 2008. Within a two-thirds random sample (Developmental cohort), we developed 2 parsimonious multivariable models to predict all-cause 30-day readmission, the first incorporating only variables known before cardiac catheterization (pre-PCI model), and the second incorporating variables known at discharge (Discharge model). Models were validated within the remaining one-third sample (Validation cohort), and model discrimination and calibration were assessed. Of 36 060 PCI patients surviving to discharge, 3760 (10.4%) patients were readmitted within 30 days. Significant pre-PCI predictors of readmission included age, female sex, Medicare or State insurance, congestive heart failure, and chronic kidney disease. Post-PCI predictors of readmission included lack of &bgr;-blocker prescription at discharge, post-PCI vascular or bleeding complications, and extended length of stay. Discrimination of the pre-PCI model (C-statistic=0.68) was modestly improved by the addition of post-PCI variables in the Discharge model (C-statistic=0.69; integrated discrimination improvement, 0.009; P<0.001). Conclusions—These prediction models can be used to identify patients at high risk for readmission after PCI and to target high-risk patients for interventions to prevent readmission.

Thrombectomy using suction filtration and veno-venous bypass: single center experience with a novel device.

To describe the first single center experience with a novel aspiration thrombectomy device.

Sources of Hospital Variation in Short-Term Readmission Rates After Percutaneous Coronary Intervention

Background— Risk-standardized all-cause 30-day readmission rates (RSRRs) after percutaneous coronary intervention (PCI) have been endorsed as a national measure of hospital quality. Little is known about variation in the performance of hospitals on this measure, and whether high hospital rates of readmission after PCI are due to modifiable deficiencies in quality of care has not been assessed. Methods and Results— We estimated 30-day, all-cause RSRRs for all nonfederal PCI-performing hospitals in Massachusetts, adjusted for clinical and angiographic variables, between 2005 and 2008. We assessed if differences in race, insurance type, and PCI and post-PCI characteristics, including procedural complications and discharge characteristics, could explain variation between hospitals using nested hierarchical logistic regression models. Of 36 060 patients undergoing PCI at 24 hospitals and surviving to discharge, 4469 (12.4%) were readmitted within 30 days of discharge. Hospital RSRRs ranged from 9.5% to 17.9%, with 8 of 24 hospitals being identified as outliers (4 lower than expected and 4 higher than expected). Differences in race, insurance, PCI, and post-PCI factors accounted for 10.4% of the between-hospital variance in RSRRs. Conclusions— We observed wide variation in hospital 30-day all-cause RSRRs after PCI, most of which could not be explained by identifiable differences in procedural and postprocedural factors. A better understanding of etiologies of hospital variation is necessary to determine whether this measure is an actionable assessment of hospital quality, and, if so, how hospitals might improve their performance.

Furthering the Link Between the Sarcomere and Primary Cardiomyopathies: Restrictive Cardiomyopathy Associated with Multiple Mutations in Genes Previously Associated With Hypertrophic or Dilated Cardiomyopathy

Mutations in genes that encode components of the sarcomere are well established as the cause of hypertrophic and dilated cardiomyopathies. Sarcomere genes, however, are increasingly being associated with other cardiomyopathies. One phenotype more recently recognized as a disease of the sarcomere is restrictive cardiomyopathy (RCM). We report on two patients with RCM associated with multiple mutations in sarcomere genes not previously associated with RCM. Patient 1 presented with NYHA Class III/IV heart failure at 22 years of age. She was diagnosed with RCM and advanced heart failure requiring heart transplantation. Sequencing of sarcomere genes revealed previously reported homozygous p.Glu143Lys mutations in MYL3, and a novel heterozygous p.Gly57Glu mutation in MYL2. The patients mother is a double heterozygote for these mutations, with no evidence of cardiomyopathy. Patient 2 presented at 35 years of age with volume overload while hospitalized for oophorectomy. She was diagnosed with RCM and is being evaluated for heart transplantation. Sarcomere gene sequencing identified homozygous p.Asn279His mutations in TPM1. The patients parents are consanguineous and confirmed heterozygotes. Her father was diagnosed with HCM at 42 years of age. This is the first report of mutations in TPM1, MYL3, and MYL2 associated with primary, non‐hypertrophied RCM. The association of more sarcomere genes with RCM provides further evidence that mutations in the various sarcomere genes can cause different cardiomyopathy phenotypes. These cases also contribute to the growing body of evidence that multiple mutations have an additive effect on the severity of cardiomyopathies.