Treatment With Cardiovascular Medications: Prognosis in Patients With Myocardial Injury

Abstract

Background There is no clinical guidance on treatment in patients with non‐ischemic myocardial injury and type 2 myocardial infarction (T2MI). Methods and Results In a cohort of 22 589 patients in the emergency department at Karolinska University Hospital in Sweden during 2011 to 2014 we identified 3853 patients who were categorized into either type 1 myocardial infarction, T2MI, non‐ischemic acute and chronic myocardial injury. Data from all dispensed prescriptions within 180 days of the visit to the emergency department were obtained concerning β‐blockers, angiotensin‐converting enzyme inhibitors/angiotensin II receptor blockers, statins, and platelet inhibitors. We estimated adjusted hazard ratios (HR) with 95% CI for all‐cause mortality in relationship to the number of medications (categorized into 0–1 [referent], 2–3 and 4 medications) in the groups of myocardial injury. In patients with T2MI, treatment with 2 to 3 and 4 medications was associated with a 50% and 56% lower mortality, respectively (adjusted HR [95% CI], 0.50 [0.25–1.01], and 0.43 [0.19–0.96]), while corresponding associations in patients with acute myocardial injury were 24% and 29%, respectively (adjusted HR [95% CI], 0.76 [0.59–0.99] and 0.71 [0.5–1.02]), and in patients with chronic myocardial injury 27% and 37%, respectively (adjusted HR [95% CI], 0.73 [0.58–0.92] and 0.63 [0.46–0.87]). Conclusions Patients with T2MI and non‐ischemic acute or chronic myocardial injury are infrequently prescribed common cardiovascular medications compared with patients with type 1 myocardial infarction. However, treatment with guideline recommended drugs in patients with T2MI and acute or chronic myocardial injury is associated with a lower risk of death after adjustment for confounders.

Associations of kidney tests at medical facilities and health checkups with incidence of end-stage kidney disease: a retrospective cohort study

“…Use of these drugs was determined based on the history of one or more prescriptions during the 6 months prior to the baseline date. The medical claims codes for drugs were converted to Anatomical Therapeutic Chemical (ATC) Classification System codes using the master data developed by the Japan Pharmaceutical Information Center ( http://www.japic.or.jp ) to identify anti-diabetic (ATC codes: A10) 22 , anti-hypertensive (C03A, C07, C08, and C09) 22 , lipid-lowering (C10AA, C10AX09, and C10BA) 23 , and anti-platelet drugs (B01AC) (Supplementary Table S2 ) 24 . Smoking status was classified into the absence and presence of current smoking using a health checkup questionnaire.…”

Type 2 myocardial infarction: a diagnostic and therapeutic challenge in contemporary cardiology

“…Interestingly, however, the heightened diagnostic potential of high-sensitivity cTn has not translated into better outcomes, perhaps because physicians are still reluctant to interpret mild cTn elevations as proper MIs and treat them appropriately. This observation is particularly valid for T2MI, as under its umbrella completely different pathological processes fall [9,10]. In addition, fewer than two-thirds of patients with T2MI are referred to a cardiology consultation, and most of them do not have any outpatient follow-up after discharge [11].…”

“…The only possible management of T2MI is a causal therapy of its associated conditions through a phenotype-specific approach, once the patient has been stabilised and the trigger has been corrected or controlled [25,29]. Currently, it is not possible to formulate definite recommendations because of the minimal evidence resulting from observational and retrospective studies, which should be interpreted as hypothesis-generating only [10,36]. According to a single-centre study, the use of evidence-based medicines in T2MI can halve mortality, but these data need stronger validation [10].…”

A review on the molecular basis underlying the protective effects of Andrographis paniculata and andrographolide against myocardial injury

“…56 The PI3K/Akt pathway is triggered by the engagement of receptor tyrosine kinase or Toll-like receptor with their respective ligands. PI3K is recruited and activated, facilitating the conversion of phosphatidylinositol (3,4)-bisphosphate (PIP 2 ) to phosphatidylinositol (3,4,5)-trisphosphate (PIP 3 ) and subsequent phosphorylation of Akt. Eventually, the activated Akt promotes inflammatory response.…”

“…1 Treatment strategies for type I myocardial infarction are well established, but there is no clinical guidance or recommended therapy for patients with other myocardial injury categories. 2,3 These shortcomings prompt the search for alternative agents to manage myocardial injury.…”