STEMI and NSTEMI: the dangerous brothers.

Ever since the redefinition of myocardial infarction (MI) inthe year 2000,¹ a new entity has entered the field: non-ST-elevationMI (NSTEMI). STEMI and NSTEMI share the release of specificmyocardial necrosis markers which define them clinically asacute MI (AMI) and set them apart from unstable angina, an acutecoronary syndrome which does not qualify as MI. NSTEMI: getting to know the younger brother With the creation of     

Recent trends in the incidence, treatment, and outcomes of patients with STEMI and NSTEMI

Background

Despite the widespread use of electrocardiographic changes to characterize patients presenting with acute myocardial infarction, little is known about recent trends in the incidence rates, treatment, and outcomes of patients admitted for acute myocardial infarction further classified according to the presence of ST-segment elevation. The objectives of this population-based study were to examine recent trends in the incidence and death rates associated with the 2 major types of acute myocardial infarction in residents of a large central Massachusetts metropolitan area.

Methods

We reviewed the medical records of 5383 residents of the Worcester (MA) metropolitan area hospitalized for either ST-segment elevation acute myocardial infarction (STEMI) or non-ST-segment acute myocardial infarction (NSTEMI) between 1997 and 2005 at 11 greater Worcester medical centers.

Results

The incidence rates (per 100,000) of STEMI decreased appreciably (121 to 77), whereas the incidence rates of NSTEMI increased slightly (126 to 132) between 1997 and 2005. Although in-hospital and 30-day case-fatality rates remained stable in both groups, 1-year postdischarge death rates decreased between 1997 and 2005 for patients with STEMI and NSTEMI.

Conclusions

The results of this study demonstrate recent decreases in the magnitude of STEMI, slight increases in the incidence rates of NSTEMI, and decreases in long-term mortality in patients with STEMI and NSTEMI. Our findings suggest that acute myocardial infarction prevention and treatment efforts have resulted in favorable decreases in the frequency of STEMI and death rates from the major types of acute myocardial infarction.     

The impact of admission plasma glucose on long-term mortality after STEMI and NSTEMI myocardial infarction

Diabetes mellitus is a widely recognized risk factor for cardiovascular disease. Type 2 diabetics have a 3-fold increased risk of CAD; prediabetics, without chronic hyperglycemia, have a 2-fold increased risk compared with normal subjects. We determined in 615 consecutive acute infarction patients whether the admission plasma glucose level remains associated with major adverse cardiovascular events (MACE) in an unselected patient population with myocardial infarction. Of these, the mean age of 66+/-12 years (range 36-90) and 69% were men and mean APG and HbA1c level were 8.2+/-4.0 mmol/l and 6.1+/-1.1% respectively. 13.2% of total study population was already known with diabetes. We recorded 132 deaths (21.5%), of whom 23.6% were known diabetic patients during 2.5 years of follow-up Multivariate statistical analysis identified APG, older age and previous MI as independent mortality predictors. CONCLUSION: Increased APG levels are significantly and independently correlated with poor prognosis after myocardial infarction, and this underlines the need for better medical treatment of hyperglycemic state and aggressive screening for early detection of diabetes.     

Increased Vulnerability and Distinct Layered Phenotype at Culprit and Nonculprit Lesions in STEMI Versus NSTEMI

ObjectivesThis study aimed to investigate the pancoronary plaque vulnerability (including culprit and nonculprit lesions) and layered phenotype in patients with ST-segment elevation myocardial infarction (STEMI) vs non-STEMI (NSTEMI).BackgroundPancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis.MethodsA total of 464 patients with AMI who underwent 3-vessel optical coherence tomography imaging were consecutively studied and divided into a STEMI group (318 patients; 318 culprit and 1,187 nonculprit plaques) and a NSTEMI group (146 patients; 146 culprit and 560 nonculprit plaques). Patients were followed up for a median period of 2 years.ResultsCompared with NSTEMI, culprit lesions in STEMI had more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels. The prevalence of plaque rupture (8.2% vs 4.8%; P = 0.018), microvessels (57.5% vs 45.2%; P < 0.001), and calcification (40.7% vs 30.2%; P = 0.003) at nonculprit lesions was higher in STEMI than NSTEMI. The layer area and thickness at the culprit and nonculprit lesions were significantly larger in STEMI than in NSTEMI. Multivariate analyses showed that culprit layer area (odds ratio: 1.443; 95% CI: 1.138-1.830; P = 0.002) was predictive of STEMI (vs NSTEMI), in addition to culprit TCFA, culprit thrombus, and non–left circumflex artery location of the culprit lesion. Although the type of AMI was not related to clinical outcomes, high-sensitivity C-reactive protein, culprit calcified nodule, and nonculprit TCFA predicted the 2-year major adverse cardiovascular events in patients with AMI.ConclusionsPatients with STEMI had increased plaque vulnerability (ie, more plaque rupture and microvessels) and distinct layered phenotype at the culprit and nonculprit lesions compared with patients with NSTEMI. Culprit lesion features of large layer area, TCFA, thrombus, and non–left circumflex artery location predicted the clinical presentation of STEMI.     

Osteoarticular manifestations of pustulosis palmaris et plantaris and of psoriasis: two distinct entities.

OBJECTIVE: To test the hypothesis that pustulosis palmaris et plantaris and psoriatic arthritis (PsA) are two distinct diseases, and that the associated dermatoses are therefore also distinct diseases. METHODS: We prospectively performed clinical, radiological, biological, and bone scan investigations in 23 outpatients with pustolotic arthritis and 23 outpatients with PsA, matched by gender, age (+/- one year) and duration of arthritis (+/- two years). RESULTS: The anterior chest wall, especially the sternocostoclavicular joints, was more frequently involved in pustulotic arthritis than in PsA, both clinically (82% v 43%; p < 0.001) and radiologically (47% v 17%; p < 0.05). Sternocostoclavicular joints generally presented with erosive lesions in PsA, and with large ossifications in pustulotic arthritis. Peripheral joint involvement was mono- or oligoarticular, affecting proximal joints, in pustulotic arthritis (74% v 21%; p < 0.01), and polyarticular, involving small distal joints, in PsA (60% v 0%; p < 10(-4)), in which condition it was also more often erosive (43% v 8%; p < 0.01). The frequency of sacroiliitis and of spine involvement was similar in pustulotic arthritis and PsA. Biology and bone scan did not help distinguish between the two groups. CONCLUSIONS: Pustulotic arthritis and PsA are clinically and radiologically different, therefore pustulosis palmaris et plantaris and psoriasis are most probably distinct dermatological diseases.     

Primarily chronic progressive and relapsing/remitting multiple sclerosis: two immunogenetically distinct disease entities

HLA class II gene polymorphism was investigated in 100 patients with clinically definite multiple sclerosis (MS) by restriction fragment length polymorphism analysis of Taq I-digested DNA using DRB, DQA, and DQB cDNA probes. Twenty-six patients had primarily chronic progressive MS and 74 had relapsing/remitting MS. The latter group included patients with a secondary progressive evolution of symptoms. Both clinical forms of MS were found to be associated with the DRw15,DQw6 haplotype. In addition, primarily chronic progressive MS was positively associated with the DQB1 restriction fragment pattern seen in DR4,DQw8, DR7,DQw9, and DRw8, DQw4 haplotypes, as well as negatively associated with the Taq I DQB1 allelic pattern corresponding to the serological specificity DQw7. Relapsing/remitting MS was positively associated with the DQB1 allelic pattern observed in the DRw17,DQw2 haplotype. These three DQB1 alleles are in strong negative linkage disequilibria with DRw15. The two susceptibility markers of each clinical form of MS act additively in determining the genetic susceptibility, as the relative risks for individuals carrying both markers roughly equal the sum of respective risks. Different alleles of the DQB1 locus defined by restriction fragment length polymorphisms contribute to susceptibility and resistance to primarily chronic progressive MS as well as to susceptibility to relapsing/remitting MS. The observed immunogenetic heterogeneity between the different clinical forms of MS favors the hypothesis that primarily chronic progressive MS and relapsing/remitting MS are two distinct disease entities.     

Giant colonic diverticula—Three distinct entities

A case report and review of the literature support a new theory that giant colonic diverticula are three distinct pathologic entities. The three types can be separated by histologic type.     

Using the Gensini score to estimate severity of STEMI,NSTEMI, unstable angina,and anginal syndrome

Gensini score (GS) provides valuable information on severity and prognosis of coronary artery disease (CAD).To evaluate the relationship between the severity of CAD determined by the GS and relation to ST-elevation myocardial infarction, non-ST segment elevation myocardial infarction (NSTEMI), unstable angina pectoris, chest pain (suspected angina syndrome on admission) and risk-factors for CAD and predictors of severity.Observational cross-sectional study.Consecutive patients who underwent clinically-indicated coronary angiography for ST-elevation myocardial infarction, NSTEMI, unstable angina pectoris or chest pain were enrolled.Among 600 patients, 417 (average age 67.8 ± 12.2 years) had CAD–related symptoms. Mean GS was 66.7 ± 63.8. Patients presenting with NSTEMI had the highest GS (81.3 ± 42.3; P < .001) Regression analysis of risk-factors showed the best association of GS with multivessel disease and coronary artery bypass graft. Regression analysis of medications showed that clopidogrel, had the best association with low GS.GS correlated with the severity of CAD, multivessel disease, coronary artery bypass graft, and troponin. GS was related to the cardiovascular risk-factors of diabetes, hypertension, and high-density cholesterol.     

Type I pseudohypoaldosteronism includes two clinically and genetically distinct entities with either renal or multiple target organ defects

Type I pseudohypoaldosteronism (PHA) is a hereditary disease characterized by salt wasting resulting from target organ unresponsiveness to mineralocorticoids. We have studied two kindreds including a total of nine patients with PHA. In kindred I, the propositus presented with renal salt wasting in infancy (vomiting, failure to thrive, short stature, hyponatremia, hyperkalemia) and responded dramatically to a high salt diet (2.5 g/day). Sodium supplementation was discontinued at the age of two. In seven additional family members from three generations, clinical expression of PHA varied from asymptomatic to moderate. In affected members (propositus, mother, and two brothers), hyperaldosteronism persisted over 13 yr; however, the PRA decreased gradually to near normal values. Persistent hyperaldosteronism in the face of a decrease in PRA indicated the development of tertiary hyperaldosteronism due to autonomously functioning zona glomerulosa. The pedigree was consistent with an autosomal dominant mode of transmission with variable expression. In kindred II, the propositus, who was the product of a consanguineous marriage, developed severe renal salt losing at age 9 days. She had also increased salivary and sweat electrolytes consistent with PHA resulting from multiple organ unresponsiveness to mineralocorticoids. Life threatening episodes of salt wasting recurred beyond the age of 2 yr. At 5 yr of age she still requires high amounts of salt supplements (14 g/day). A sister died at 9 days of age with PHA symptoms. Six close relatives (parents, three siblings, maternal uncle) showed no biochemical abnormalities. This pedigree was consistent with an autosomal recessive mode of inheritance. In view of the findings on these two kindreds and the analysis of those in the literature, we conclude that type I PHA includes two clinically and genetically distinct entities with either renal or multiple target organ defects.     

Two distinct pathophysiological mechanisms in congenital nephrogenic diabetes insipidus

V1 and V2 vasopressin receptor functions were studied in 2 patients with congenital nephrogenic diabetes insipidus. V1 receptor-mediated functions (increase in urinary prostaglandin E2 excretion and plasma cortisol levels) and Gs (guanine nucleotide-binding stimulatory protein) activity of erythrocyte membranes were normal in both patients. After infusion of 0.4 micrograms/kg dDAVP, a 57-yr-old male patient had no increase in plasma factor VIII coagulant, ristocetin cofactor, or fibrinolytic activity or change in von Willebrand factor multimers. In addition, he had no vasodilatory response to dDAVP, a response that occurs in normal subjects and patients with central diabetes insipidus. In contrast, a 25-yr-old female patient had normal hemostatic and vasodilatory responses to the infusion of dDAVP. These observations indicate that the cellular abnormalities in patients with congenital nephrogenic diabetes insipidus may be either at the V2 receptor or in the postreceptor (and Gs activity) cascade of events that mediate vasopressin-induced antidiuresis. Therefore, heterogeneity exists in the biochemical cause(s) of congenital nephrogenic diabetes insipidus in man.     

STEMI and NSTEMI: are they so different? 1 year outcomes in acute myocardial infarction as defined by the ESC/ACC definition (the OPERA registry).

AIMS: The ESC/ACC redefined myocardial infarction as any amount of necrosis caused by ischaemia. The aim of this study was to describe the management and outcomes using 'real-world' data taking the new definition of acute myocardial infarction into account. METHODS AND RESULTS: A total of 2,151 consecutive patients (76.0% men) with a myocardial infarction were enrolled at 56 centres in France. The median delay to presentation was shorter in patients with ST-segment elevation myocardial infarction (STEMI) vs. non-STEMI (NSTEMI) (4 vs. 7 h, P < 0.0001). STEMI patients were more likely to receive fibrinolysis (28.9 vs. 0.7%, P < 0.0001) or undergo PCI (71.0 vs. 51.6%, P < 0.0001) but less likely to have bypass surgery (3.1 vs. 4.9%, P < 0.05). At discharge, patients with STEMI received more aggressive secondary prevention therapies than those with NSTEMI, which was not supported by differences in disease severity. A total of 1878 patients were followed-up for 1 year: 36.7% of STEMI and 41.5% of NSTEMI patients were rehospitalized (P = 0.05); 16% in both groups were revascularized. In-hospital mortality was similar (4.6 vs. 4.3%), and 1-year mortality was 9.0% in STEMI patients and 11.6% in NSTEMI patients (Log-Rank P = 0.09). Independent correlates of in-hospital mortality were untreated dyslipidaemia, advanced age, diabetes, and low blood pressure. The strongest predictors of 1-year mortality were heart failure and age. Similar predictors were found in STEMI and NSTEMI subgroups. CONCLUSIONS: Despite different management, patients with STEMI and NSTEMI have similar prognoses and independent correlates of outcome. These findings support the new definition of myocardial infarction.     

The impact of unsuccessful percutaneous coronary intervention on short‐ and long‐term prognosis in STEMI and NSTEMI

Objectives: To compare the impact of the efficacy of percutaneous coronary intervention (PCI) on prognosis in ST and non‐ST elevation myocardial infarction (STEMI and NSTEMI) patients with respect to infarct‐related artery (IRA). Background: The significance of the efficacy of PCI in STEMI and NSTEMI depending on the type of IRA has yet to be clarified. Methods: Study population consisted of 2,179 STEMI and 554 NSTEMI consecutive patients treated with urgent PCI. The efficacy of PCI (TIMI [thrombolysis in myocardial infarction] 3 vs. TIMI < 3) was assessed with regard to the type of IRA (left anterior descending artery, circumflex artery [Cx] or right coronary artery). The mean follow‐up was 37.5 months. Results: The rate of unsuccessful PCI was similar in STEMI and NSTEMI irrespectively of IRA (14.1 vs. 17.7%; P = 0.062). In STEMI, unsuccessful PCI was associated with significantly higher early (23.1 vs. 5.6%; P < 0.001) and late (29.9 vs. 12.8%; P < 0.001) mortality regardless of IRA. In NSTEMI, the inefficacious PCI significantly increased early (19.0% vs. 0.9%; P < 0.001) and late (27.3% vs. 6.3%; P < 0.001) mortality only in patients with Cx‐related infarction. Unsuccessful PCI of IRA was an independent risk factor for death in STEMI (HR 1.64; P < 0.05), but not in NSTEMI (P = 0.64). Further analysis showed that whilst unsuccessful PCI of any vessel in STEMI is an independent risk factor for death, in NSTEMI this applies to unsuccessful PCI of Cx only. Conclusions: The significance of unsuccessful PCI of IRA seems to be different in STEMI and NSTEMI. Unsuccessful PCI is an independent risk factor for death in STEMI regardless of IRA and in NSTEMI with the involvement of Cx. © 2010 Wiley‐Liss, Inc.     

External validation, extension and recalibration of Braunwald's simple risk index in a community-based cohort of patients with both STEMI and NSTEMI

BACKGROUND: Using the simple risk index (SRI) that is based on age, heart rate and systolic blood pressure, we sought to evaluate the ability to predict outcome in AMI patients in a community-based population. METHODS AND RESULTS: We identified and evaluated 3684 consecutive patients with an admission diagnosis of possible AMI, who attended between 1st September and 30th November 1995. Two thousand one hundred fifty three patients had confirmed evidence of WHO definition AMI, of whom 1656 survived to hospital discharge. We evaluated the ability of the SRI to predict mortality over 30 days using the score generated by the equation (heart ratex[age/10]2)/systolic blood pressure. The SRI was a strong (c-statistic = 0.77 CI 0.74-0.79) predictor of 30-day mortality in both STEMI and all consecutive cases of WHO definition AMI. However, the model showed poor calibration when used on a community-based population with 30-day mortality being underestimated across all risk quintiles. Consequently we sought to recalibrate the quantitative aspects of the model for the total AMI population in the following way (Risk Index; 30-day mortality) (< or = 29.2; 9.2%), (29.3-37.8; 23.9%), (37.9-47.3; 34.6%), (47.4-61.5; 40.3%), (> or = 61.6; 65.5%). CONCLUSION: We have externally validated the SRI in an unselected cohort of consecutive WHO definition AMI patients. However, the original model consistently underestimated the likelihood of death at 30 days regardless of the calculated risk score. We have therefore suggested corrections to the risk estimates, to allow its application in an unselected community cohort.     

HbA2 levels in normal adults are influenced by two distinct genetic mechanisms

Using a genome‐wide association study, we found that common inter‐individual differences in haemoglobin A₂ (HbA₂, α₂δ₂) levels are largely governed by genetic factors (42% of variability). The influence of age (1%) and sex (4%) was small. HbA₂ levels were influenced by two loci: the HBS1L‐MYB locus on chromosome 6q, which has been shown to have pleiotropic effects on other haematological traits; and a second locus surrounding HBB, the gene encoding β‐globin. Our results suggest that HbA₂ levels in adults are influenced by two different biological processes: one via kinetics of erythropoiesis, and the other, via competition between HBB and HBD activity.     

Centrilobular and panlobular emphysema in smokers. Two distinct morphologic and functional entities.

In order to investigate the hypothesis that different morphologic patterns of disease might correspond to different mechanical properties of the lung in emphysema, pulmonary function tests and lung mechanics were measured in 34 subjects undergoing lung resection for peripheral lung tumors. Using standard microscopic criteria, pure or predominant centrilobular (n = 18) or panlobular (n = 16) emphysema was diagnosed in lungs. The degree of emphysema measured by the mean linear intercept (Lm) was not significantly different between the two groups. However, the coefficient of variation of the interalveolar wall distance (CV) was significantly higher for the same Lm in CLE than in PLE. This indicates that CLE has an uneven pattern of destruction, whereas PLE is more homogeneous. CLE had a higher degree of abnormalities in the small airways (SAD) than did PLE (p less than 0.05) mainly because of significantly higher muscle score (p less than 0.001) and fibrosis. CLE also had a higher proportion of airways less than 400 microns in diameter than did PLE (p less than 0.05). Static compliance, specific compliance, and the exponential constant (K) were significantly lower (p less than 0.005, p less than 0.001, and p less than 0.05, respectively) in CLE than in PLE. FEV1/FVC was significantly correlated with SAD in CLE (r = -0.69, p less than 0.01) but not in PLE (r = 0.29 p greater than 0.05); conversely, FEV1/FVC was significantly correlated with elasticity (K) in PLE (r = -0.72, p less than 0.01) but not in CLE (r = 0.08, p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)