Cocaine Positivity in ST-Elevation Myocardial Infarction: A True or False Association.

INTRODUCTION: Every year, more than 500,000 US Emergency Department visits are associated with cocaine use. People who use cocaine tend to have a lower incidence of true ST-elevation myocardial infarction (STEMI). OBJECTIVE: To identify the factors associated with true STEMI in patients with cocaine-positive (CPos) findings. METHODS: We retrospectively analyzed 1144 consecutive patients with STEMI between 2008 and 2013. True STEMI was defined as having a culprit lesion on coronary angiogram. Multivariate and univariate analyses were used to identify risk factors and create a predictive model. RESULTS: A total of 64 patients with suspected STEMI were CPos (mean age 53.1 ± 11.2 years; male = 80%). True STEMI was diagnosed in 34 patients. Patients with CPos true STEMI were more likely to be uninsured than those with false STEMI (61.8% vs 34.5%, p = 0.03) and have higher peak troponin levels (21.1 ng/mL vs 2.12 ng/mL, p = < 0.01) with no difference in mean age between the 2 groups (p = 0.24). In multivariate analyses, independent predictors of true STEMI in patients with CPos findings included age older than 65 years (odds ratio [OR] = 19.3, 95% confidence iterval [CI] = 1.2-318.3), lack of health insurance (OR = 4.9, 95% CI = 1.2-19.6), and troponin level higher than 0.05 (OR = 24.0, 95% CI = 2.6-216.8) (all p < 0.05). A multivariate risk score created with a C-statistic of 82% (95% CI = 71-93) significantly improved the identification of patients with true STEMI. CONCLUSION: Among those with suspected STEMI, patients with CPos findings had a higher incidence of false STEMI. Older age, lack of health insurance, and troponin levels outside of defined limits were associated with true STEMI in this group.

Safety and efficacy of switching from unfractionated heparin to bivalirudin during primary percutaneous coronary intervention.

OBJECTIVES: To evaluate the safety and efficacy of switching to bivalirudin during primary percutaneous coronary intervention (PCI) for patients who received preprocedure unfractionated heparin (UFH). BACKGROUND: Current guidelines favor bivalirudin for primary PCI in patients at high risk of bleeding, particularly when femoral access is used. However, patients with ST-segment elevation myocardial infarction frequently receive UFH before arrival in the catheterization laboratory. METHODS: Scientific databases and websites were searched for randomized controlled trials. Patients were divided into those who received heparin with or without glycoprotein IIb/IIIa inhibitors (heparin group); those switched to bivalirudin during primary PCI from preprocedure UFH (switch group); and those who received bivalirudin without preprocedure UFH (Biv-alone group). Both traditional pairwise meta-analyses using moderator analyses and network meta-analyses using mixed-treatment comparison models were performed. RESULTS: Data from five trials including13,547 patients were analyzed. In mixed-comparison models, switching to bivalirudin during primary PCI was associated with lower rates for all-cause mortality and major adverse cardiovascular events (MACEs) compared to the other strategies. Rates for all-cause mortality, MACEs, and net adverse clinical events (NACEs) were similar for the heparin and Biv-alone groups. Switching strategies was also associated with lower major bleeding rates compared to heparin alone. Similarly, in a standard pairwise model, both the switch and Biv-alone groups were associated with decreased bleeding risk compared to the heparin group. However, only the switch strategy was associated with decreased all-cause mortality (RR, 0.47; 95% CI, 0.30-0.75; P = 0.001), MACE (RR, 0.67; 95% CI, 0.49-0.91; P = 0.012), and NACE (RR, 0.61; 95% CI, 0.41-0.92; P = 0.019) compared with heparin alone. CONCLUSIONS: During primary PCI, use of bivalirudin for those receiving preprocedure UFH was associated decreased rates for major bleeding, NACEs, MACEs, and all-cause mortality compared to heparin +/- GPI. This strategy was also associated with decreased rates for MACEs and all-cause mortality compared to bivalirudin alone without preprocedure UFH.

Outcomes of Percutaneous Antegrade Intraluminal Coronary Intervention of Chronic Total Occlusion With Remote Surgical Backup.

Percutaneous coronary intervention (PCI) of chronic total occlusion (CTO) is not favored in facilities without on-site surgical backup. We reviewed outcomes of patients who had CTO intervention with remote surgical backup in our institution. All patients who underwent attempted antegrade intraluminal CTO PCI from January 2013 to July 2017 were analyzed. Twenty cases (18 patients, 58.1 ± 7.0 years, 70% males) were identified. Procedure was successful in 85% (17 of 20). There were 2 nonflow limiting dissections and 1 wire perforation. Two patients had post-PCI myocardial infarction. There was no cardiac death, myocardial infarction, target vessel revascularization, or stroke at 30 days and at mean follow-up of 19.5 ± 13.7 months. There were 4 rehospitalizations for angina requiring repeat angiogram in 3 cases: 2 without intervention, and 1 referred for coronary artery bypass grafting. Careful attempt at antegrade intraluminal CTO intervention done at a center with remote surgical backup is feasible in selected patients.

Double conduction through the atrioventricular node following acute medullary infarction: a case report.

Lateral medullary syndrome (LMS), also known as Wallenberg's syndrome, PICA syndrome, results from occlusion of the posterior inferior cerebellar artery, with associated infarction of parts of medulla oblongata, and cerebellum on the ipsilateral side. It often manifests as various patterns of sensory, motor, and autonomic deficits. While sensorimotor dysfunction presents as a predicted pattern of clinical signs and symptoms, autonomic dysfunction is usually less clinically apparent, and can be easily mistaken as a concomitant pathology in the end organ it affects. In this case, we present a case of an unusual pattern of cardiac arrhythmia as the first objective finding of LMS, caused by autonomic instability following infarction of vagus nerve nuclei in the medulla.

Occlusion of right coronary artery by microembolization caused by excessive diagnostic catheter manipulation.

With advancing technology and newer therapeutic and diagnostic techniques, physicians are now encountering new complications or increasing frequency of known complications than before. left cardiac catheterization and coronary angiography is not an exception. As transradial cardiac catheterization is now becoming more popular, operators should be more aware of related challenges and limitations associated. Tortuous right bracheocephalic artery is an anatomical variance that makes radial catheterization more difficult, and may indeed add additional time and risk to the procedure and patient, respectively. Hence, we present this case report.

Mortality and operator experience with vascular access for percutaneous coronary intervention in patients with acute coronary syndromes: A pairwise and network meta-analysis of randomized controlled trials.

BACKGROUND: Recently, several meta-analyses of randomized controlled trials (RCTs) have shown that transradial access (TRA) reduces mortality compared to transfemoral access (TFA). However, a critical appraisal of these RCTs suggests that the findings could have resulted from a greater incidence of adverse events in the TFA groups rather than a beneficial effect of TRA. METHODS: Scientific databases and websites were searched for RCTs. Patients were divided into groups based on access type and whether the operator was a radial expert (RE) or non-radial expert (NRE). The groups were TFA-RE, TFA-NRE, TRA-RE, and TRA-NRE. Both a traditional meta-analysis and a network meta-analysis using mixed-treatment comparison models were performed. RESULTS: Data from 13 trials including 15,615 patients were analyzed. The mortality rate for TFA-RE (3.54%) was more than double compared to TFA-NRE (1.61%). In pairwise meta-analysis, TFA-RE was associated with increased risk of mortality (RR: 1.72, 95% CI: 1.13-2.62; p=0.011) compared to TFA-NRE. In subgroup analysis, TFA-RE was associated with increased mortality (RR: 1.70, 95% CI: 1.24-2.34; p=0.001) compared to TRA, but TRA-NRE was not. Similarly, in mixed comparison models, TFA-RE was associated with increased mortality compared to TRA-NRE, TRA-RE, and TFA-NRE, but TFA-NRE was not, compared to TRA-RE and TRA-NRE. CONCLUSION: Recently-reported survival differences between TRA and TFA may have been driven by adverse events in the TFA groups of the RCTs rather than a beneficial effect of TRA. This issue needs further investigation before labeling radial access a lifesaving procedure in invasively-managed patients with ACS.

Predictors of left ventricular dilatation in young adults (from the Bogalusa Heart Study).

Left ventricular (LV) dilatation may be an early sign of cardiac decompensation progressing to LV dysfunction. Determinants of LV dilatation in young asymptomatic adults are unknown. Five hundred six asymptomatic subjects (mean age 32 +/- 3 years) enrolled in the Bogalusa Heart Study underwent echocardiographic examination. LV dilatation (LV end-diastolic diameter >5.5 cm) as measured by M-mode echocardiography was found in 31 subjects (6%). Subjects with LV dilatation had greater body mass indexes (32 +/- 9 vs 27 +/- 6 kg/m2, p <0.0001), systolic (119 +/- 15 vs 112 +/- 12 mm Hg, p = 0.007) and diastolic (79 +/- 12 vs 75 +/- 9 mm Hg, p = 0.04) blood pressures, and LV mass (230 +/- 50 vs 123 +/- 39 g, p <0.0001). Age, gender, race, and metabolic parameters (glucose, insulin, and lipoprotein levels) did not differ significantly between the subjects with and without LV dilatation. After correction for age, gender, and race differences, adulthood obesity (body mass index >30 kg/m2) was associated with a threefold odds ratio (2.9, 95% confidence interval 1.4 to 6.1), and hypertension (defined as per the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) was also associated with a threefold odds ratio (3.0, 95% confidence interval 1.2 to 7.1) for an increased incidence of LV dilatation. There was an incremental increase in LV end-diastolic dimension depending on the presence of hypertension or obesity, and subjects with obesity and hypertension in adulthood had the greatest degree of LV end-diastolic dimensions. In multiple regression analyses, body mass index in childhood was the only significant predictor of LV dilatation in adulthood (odds ratio 1.47, 95% confidence interval 1.03 to 2.09). In conclusion, obesity beginning in childhood and obesity and hypertension in young adulthood are predictors of LV dilatation in an otherwise healthy young adult population.

Donor or recipient hepatitis B seropositivity is associated with allograft vasculopathy.

BACKGROUND: Increasing interest has focused on possible viral triggers of cardiac allograft vasculopathy. Although much interest has centered on cytomegalovirus, it has recently been noted that donor hepatitis C seropositivity is associated with risk for accelerated vasculopathy. The current study hypothesized that hepatitis B (HBV) might be associated with accelerated vasculopathy. METHODS: Sixty-six patients who received heart transplants between September 1998 and July 2000 were analyzed by intravascular ultrasound within 6 weeks and again at 12 months after transplantation. These patients were divided into 2 groups: the HBV Group (n = 13) in which either the donor or recipient was seropositive for hepatitis B core antibody (HBcAb), and a Control Group (n = 53) in which neither donor nor recipient was positive for HBcAb. RESULTS: Baseline characteristics of the 2 groups were similar. The HBV Group had significant increase in the change in average intimal area (1.59 +/- 1.4 vs 0.46 +/- 0.4 mm2, p = 0.01) per mm length of the vessel compared with controls. Allograft vasculopathy at 1 year (defined as largest maximal intimal thickness increase of > or =0.50 mm) occurred in 46% of the HBV group compared with 24% of the control group (p = 0.05). When measured as an average maximal intimal thickness increase of >0.30 mm, allograft vasculopathy at 1 year occurred in 31% of the HBV Group compared with 5% of Controls (p = 0.01). CONCLUSIONS: These preliminary results suggest that HBV seropositivity in donor or recipient may be associated with an increased risk for cardiac allograft vasculopathy.

Cardiac angiotensin II receptors as predictors of transplant coronary artery disease following heart transplantation.

AIMS: We tested the hypothesis that cardiac angiotensin II (Ang II) receptor gene transcription may predict the development of transplant coronary artery disease (TCAD) following heart transplantation. METHODS AND RESULTS: We examined the gene transcripts of Ang II type 1 (AT1R) and type 2 receptors (AT2R) in endomyocardial biopsy specimens from 50 heart transplant recipients. The progression of TCAD was measured as change in maximal intimal thickness (CMIT) and change in plaque volume (CPV) by intravascular ultrasound (IVUS) examinations from baseline to one year after transplantation. The development of transplant vasculopathy was defined as a CMIT of > or = 0.3 mm over one year. The level of AT(1)R mRNA was associated with that of AT2R in transplanted hearts (regression coefficient=1.77, 95% CI 0.85-2.89, p<0.0001). AT1R and AT2R gene transcripts were univariate predictors of CMIT (AT1R: regression coefficient 0.10, 95% CI 0.06-0.14, p<0.0001; AT2R: regression coefficient 0.28, 95% CI 0.17-0.40, p<0.0001 ) or CPV (AT1R: regression coefficient 0.41, 95% CI 0.17-0.65, p<0.0001 ; AT2R: regression coefficient 1.25, 95% CI 0.49-2.01, p=0.002 ). By one year, 21 (46%) transplant recipients showed evidence of transplant vasculopathy and the rest did not. The vasculopathic group demonstrated a higher level of expression of cardiac AT1R than the non-vasculopathic group (3.7+/-2.9 vs 1.6+/-1.7 folds; p=0.006). The level of AT(1)R mRNA in transplanted heart was identified as a discriminator that predicted the development of transplant vasculopathy with a sensitivity of 75% and specificity of 83%. CONCLUSIONS: Cardiac Ang II receptor gene transcripts are associated with the progression of TCAD following heart transplantation. Only AT1R gene transcripts predicted the development of transplant vasculopathy in this preliminary study. These findings potentially support a role of Ang II receptors in the progression of TCAD following cardiac transplantation.

Donor hepatitis-C seropositivity is an independent risk factor for the development of accelerated coronary vasculopathy and predicts outcome after cardiac transplantation.

BACKGROUND: It is possible, but unproven, that hepatitis C (HCV) infection accelerates atherosclerosis. We evaluated the hypothesis that donor HCV seropositivity predicts mortality and the development of coronary vasculopathy in cardiac transplant recipients. METHODS: Thirty-four cardiac transplant recipients who were seronegative for HCV at the time of transplantation received hearts from HCV-seropositive donors. We compared the mortality and the incidence of vasculopathy in this group of patients (study group) with a group of 183 successive heart transplant recipients (control group) with no evidence of HCV in the donor or in the recipient. RESULTS: After transplantation, 75% of the HCV-seronegative patients who received hearts from HCV-seropositive donors had detectable and persistent viremia (presence of HCV-RNA by reverse-transcription polymerase chain reaction). After a mean follow-up of 4.2 +/- 1.9 years, mortality was 2.8-fold greater in the study group than in controls (95% confidence interval [CI], 1.3-5.7; p = 0.006). The risk of having any vasculopathy after a mean follow-up of 3.4 +/- 1.6 years and after adjustment for other significant risk factors was 3-fold greater (hazards ratio, 3.08; 95% CI 1.52-6.20; p = 0.001) in the HCV group compared with controls. The risk of developing advanced vasculopathy was much greater in the study group compared with controls (hazard ratio, 9.4; 97% CI, 3.3-26.6; p = < 0.0001). The risk of mortality (p = 0.005) and vasculopathy (p = < 0.0001) was greatest in patients with combined donor HCV seropositivity and the presence of antibodies against donor B cells by flow cytometry. CONCLUSION: We conclude that donor hepatitis-C virus seropositivity is an independent risk factor for increased mortality and for the development of accelerated allograft vasculopathy after cardiac transplantation. These observations may have implications for the use of HCV-positive donors in heart transplant recipients.

Computerized scoring of histopathology for predicting coronary vasculopathy, validated by intravascular ultrasound.

BACKGROUND: Allograft coronary vasculopathy results from a complex interplay between immunologic and non-immunologic factors. We devised a computerized biopsy scoring method based on histopathology to predict the development of coronary vasculopathy. METHODS: One hundred forty heart transplant recipients underwent serial intravascular ultrasound analysis at baseline (within 1 month) and at 1 year after transplantation and were evaluated for development of coronary vasculopathy (change in coronary maximal intimal thickness, CMIT). We evaluated serial endomyocardial biopsy specimens for cellular rejection, vascular rejection, ischemia, and fibrosis. In a mathematical model, we computed a biopsy score in each patient based on the duration and severity of histopathology. RESULTS: We found a significant correlation between biopsy score (RY) and progression of coronary vasculopathy (r = 0.54, p = 0.001). Using a sensitivity analysis method, an RY value of > or =560 predicted development of coronary vasculopathy with a sensitivity of 86%, specificity of 62%, and diagnostic accuracy of 80%. Compared with patients with low-risk biopsy scores (RY < 560, n = 37), patients with high-risk biopsy scores (RY > or = 560, n = 103) had increased progression of coronary vasculopathy (CMIT, 0.59 +/- 0.29 vs 0.19 +/- 0.10 mm, p < 0.001) and worse 7-year event-free survival (60% vs 91%, p = 0.01). CONCLUSION: The biopsy score is an effective method for predicting the development of coronary vasculopathy and for predicting outcome in cardiac transplant recipients.

Myocardial ischemic-fibrotic injury after human heart transplantation is associated with increased progression of vasculopathy, decreased cellular rejection and poor long-term outcome.

OBJECTIVES: We sought to assess the influence of peritransplant ischemia and fibrosis on the development of allograft vasculopathy, acute cellular rejection and long-term outcome. BACKGROUND: Allograft vasculopathy is a common long-term complication of cardiac transplantation. One of the potential risk factors is peritransplant allograft ischemia. METHODS: One hundred forty heart transplant recipients had baseline and one-year intravascular ultrasound analysis done to assess the progression of allograft vasculopathy. Serial endomyocardial biopsies were evaluated for cellular rejection, vascular rejection, ischemia and fibrosis. Based on histology, patients were classified into one of the following groups: nonischemic (n = 32), ischemia (n = 24), fibrosis (n = 62) or vascular rejection (n = 22). Three-color flow cytometry crossmatching (FCXM) was used to assess donor-specific human lymphocyte antigens (HLA) sensitization. Long-term outcome of patients in each group was assessed by estimating incidence of graft failure or deaths over a seven-year follow up. RESULTS: Patients in the fibrosis group had the lowest incidence of donor-specific HLA sensitization (40%, p = 0.008) and lowest average episodes of cellular rejection (1.7 +/- 1.4, p = 0.04), but they had increased coronary vasculopathy progression (change in coronary intimal thickness = 0.59 +/- 0.28 mm, p < 0.0001) and poor seven-year event-free survival (49%, p = 0.01). CONCLUSIONS: The development of fibrosis after cardiac transplantation is associated with advanced coronary vasculopathy, although a low incidence of acute cellular rejection is noted, suggesting the presence of nonimmune mechanisms in mediating the pathogenesis of allograft vasculopathy.