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      Impact of Type 2 Myocardial Infarction (MI) on Hospital‐Level MI Outcomes: Implications for Quality and Public Reporting

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          Abstract

          Background

          The International Classification of Diseases (ICD) coding system does not recognize type 2 myocardial infarction ( MI) as a separate entity; therefore, patients with type 2 MI continue to be categorized under the general umbrella of non–ST‐segment–elevation myocardial infarction ( NSTEMI). We aim to evaluate the impact of type 2 MI on hospital‐level NSTEMI metrics and discuss the implications for quality and public reporting.

          Methods and Results

          We conducted a single‐center retrospective analysis of 1318 patients discharged with a diagnosis of NSTEMI between July 2013 and October 2014. The Third Universal Definition was used to define type 1 and type 2 MI. Weighted Kaplan–Meier curves were used to analyze risk of mortality and readmission. Overall, 1039 patients met NSTEMI criteria per the Third Universal Definition; of those, 264 (25.4%) had type 2 MI. Patients with type 2 MI were older, were more likely to have chronic kidney disease, and had lower peak troponin levels. Compared with type 1 MI patients, those with type 2 MI had higher inpatient mortality (17.4% versus 4.7%, P<0.0001) and were more likely to die from noncardiovascular causes (71.7% versus 25.0%, P<0.0001). Despite weighting for patient characteristics and discharge medications, patients with type 2 MI had higher mortality at both 30 days (risk ratio: 3.63; 95% confidence interval, 1.67–7.88) and 1 year (risk ratio: 1.98; 95% confidence interval, 1.44–2.73) after discharge. Type 2 MI was also associated with a lower 30‐day cardiovascular‐related readmission (risk ratio: 0.49; 95% confidence interval, 0.12–2.06).

          Conclusions

          NSTEMI metrics are significantly affected by type 2 MI patients. Type 2 MI patients have distinct etiologies, are managed differently, and have higher mortality compared with patients with type 1 MI. Moving forward, it may be appropriate to exclude type 2 MI data from NSTEMI quality metrics.

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          Most cited references21

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          Adjusted survival curves with inverse probability weights.

          Kaplan-Meier survival curves and the associated nonparametric log rank test statistic are methods of choice for unadjusted survival analyses, while the semiparametric Cox proportional hazards regression model is used ubiquitously as a method for covariate adjustment. The Cox model extends naturally to include covariates, but there is no generally accepted method to graphically depict adjusted survival curves. The authors describe a method and provide a simple worked example using inverse probability weights (IPW) to create adjusted survival curves. When the weights are non-parametrically estimated, this method is equivalent to direct standardization of the survival curves to the combined study population.
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            The coronary circulation in human septic shock.

            Reversible myocardial depression, manifested by ventricular dilatation and decreased ejection fraction, is common in human septic shock. A proposed mechanism, based on animal studies, is myocardial ischemia resulting from inadequate coronary blood flow. Coronary flow observations have not been reported for human septic shock. To determine whether myocardial depression in human septic shock is associated with reduced coronary flow, thermodilution coronary sinus catheters were placed in seven patients with septic shock for measurements of coronary flow and myocardial metabolism. Four of the seven patients developed myocardial depression. These patients had coronary flow similar to or higher than that of control subjects and similar to that of the other three patients, who did not develop myocardial depression. None of the patients had net myocardial lactate production. In general, compared with values in control subjects, the oxygen content difference (arterial minus coronary sinus) was narrowed, and the fractional extraction of arterial oxygen was diminished. This pattern of disordered coronary autoregulation is analogous to the pattern of arteriovenous shunting in other organs in patients with septic shock. The preservation of coronary flow, the net myocardial lactate extraction, and the increased availability of oxygen to the myocardium argue against global ischemia as the cause of myocardial depression in human septic shock.
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              Troponin elevation in patients with heart failure: on behalf of the third Universal Definition of Myocardial Infarction Global Task Force: Heart Failure Section.

              Cardiac troponin testing is commonly performed in patients with heart failure (HF). Despite being strongly linked to spontaneous (Type I) acute myocardial infarction (MI)--a common cause of acute HF syndromes--it is well recognized that concentrations of circulating troponins above the 99 th percentile of a normal population in the context of both acute and chronic HF are highly prevalent, and frequently unrelated to Type I MI. Other mechanism(s) leading to troponin elevation in HF syndromes remain elusive in many cases but prominently includes supply-demand inequity (Type II MI), which may be associated with coronary artery obstruction and endothelial dysfunction, or may occur in the absence of coronary obstruction due to increased oxygen demand related to increased wall tension, anaemia, or other factors provoking subendocardial injury. Non-coronary triggers, such as cellular necrosis, apoptosis, or autophagy in the context of wall stress may explain the troponin release in HF, as can toxic effects of circulating neurohormones, toxins, inflammation, and infiltrative processes, among others. Nonetheless, across a wide spectrum of HF syndromes, when troponin elevation occurs, independent of mechanism, it is strongly predictive of an adverse outcome. Clinicians should be aware of the high frequency of troponin elevation when measuring the marker in patients with HF, should keep in mind the possible causes of this phenomenon, and, independent of a diagnosis of 'acute MI', should recognize the considerable ramifications of troponin elevation in this setting.
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                Author and article information

                Contributors
                saror@email.unc.edu
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                26 March 2018
                03 April 2018
                : 7
                : 7 ( doiID: 10.1002/jah3.2018.7.issue-7 )
                : e008661
                Affiliations
                [ 1 ] Division of Cardiology and McAllister Heart Institute University of North Carolina at Chapel Hill NC
                [ 2 ] Department of Epidemiology Gillings School of Global Public Health University of North Carolina at Chapel Hill NC
                [ 3 ] Division of Cardiology Brigham and Women's Hospital Harvard Medical School Boston MA
                [ 4 ] Campbell University School of Osteopathic Medicine Lillington NC
                [ 5 ] Division of Cardiology Medical College of Georgia at Augusta University Augusta GA
                [ 6 ] Piedmont Heart Institute Atlanta GA
                Author notes
                [*] [* ] Correspondence to: Sameer Arora, MD, Division of Cardiology and McAllister Heart Institute, University of North Carolina, Chapel Hill, NC 27599. E‐mail: saror@ 123456email.unc.edu
                Article
                JAH33079
                10.1161/JAHA.118.008661
                5907605
                29581221
                8fd3b709-4688-4723-bb0f-e6c12d574686
                © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 17 January 2018
                : 23 February 2018
                Page count
                Figures: 6, Tables: 3, Pages: 11, Words: 7422
                Categories
                Original Research
                Original Research
                Coronary Heart Disease
                Custom metadata
                2.0
                jah33079
                03 April 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.3.4 mode:remove_FC converted:03.04.2018

                Cardiovascular Medicine
                coronary artery disease,mortality,myocardial infarction,readmission,troponin,quality and outcomes,mortality/survival,acute coronary syndromes

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