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Acute myocardial infarction: Patients with diabetes mellitus

Acute myocardial infarction: Patients with diabetes mellitus
Literature review current through: Jan 2024.
This topic last updated: Nov 09, 2023.

INTRODUCTION — Cardiovascular events related to atherosclerotic cardiovascular disease are a major cause of morbidity and mortality among patients with diabetes mellitus. Compared with patients without diabetes, those with diabetes are more likely to have coronary heart disease and more severe multivessel coronary artery disease when it occurs. As a result of these and other factors, patients with diabetes and coronary heart disease have worse outcomes, including lower rates of long-term survival when compared with patients without diabetes who have coronary heart disease. (See "Prevalence of and risk factors for coronary heart disease in patients with diabetes mellitus".)

With respect to acute myocardial infarction (MI), including ST-elevation MI (STEMI) and non-ST-elevation MI (NSTEMI), in patients with diabetes, its treatment is broadly similar to that in those without diabetes. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

This topic will focus on a number of specific issues that should be considered in diabetic patients. The majority of data discussed in this review are related to those patients with type 2 diabetes mellitus. However, despite a paucity of data in type 1 diabetes, the general principles of care appear to also be applicable to them.

RELATIONSHIP BETWEEN DIABETES AND MYOCARDIAL INFARCTION — Diabetes is increasing in prevalence across the world and has increased from 108 million in 1980 to 422 million in 2014 [1]. Diabetes is underrecognized and it is estimated that approximately 5 percent of the population has undiagnosed diabetes [2]. While there have been overall reductions in the absolute number of acute myocardial infarctions in patients with diabetes given advances in medical therapy, these gains are threatened by the continued increase in the prevalence of diabetes [3].

It is not uncommon for the first diagnosis of diabetes to be made at the time of a MI. The incidence of newly diagnosed diabetes varies and has been found in approximately 5 percent of patients [4,5]. Other studies have found even higher prevalence of undiagnosed diabetes [6].

Similar to smoking, hypertension, and dyslipidemia, the high prevalence of diabetes in patients with acute MI relates to the fact that it is an independent risk factor for atherosclerotic heart disease. Diabetes has continued to be a significant independent risk factor for atherosclerotic heart disease. The importance of diabetes as a risk factor was illustrated in a 1998 study of the Finnish population that compared the seven-year incidence of MI in 1373 nondiabetics and 1059 patients with type 2 diabetes [7].

Patients with diabetes but no prior infarction had a similar risk of subsequent MI (20 and 19 percent, respectively) and coronary mortality (15 versus 16 percent) as nondiabetic patients with a prior MI. The risk of infarction was greatest in diabetics with a prior MI and lowest in nondiabetics without a prior MI (45 and 4 percent, respectively). While these data have led some to conclude that having diabetes increases a patient's risk of CHD events to a similar magnitude as patients with prior MI who do not have type 2 diabetes mellitus, the totality of and newer evidence does not support diabetes as a CHD equivalent. A 2009 meta-analysis found that those with diabetes but no history MI had a lower risk of cardiovascular events when compared with patients without diabetes who have had a prior MI (OR 0.56, 95% CI 0.53-0.60) [8,9].

In patients with acute MI, those with diabetes have significantly higher risk of subsequent mortality and future cardiovascular events [10]. Furthermore, there appears to be a graded rise in cardiovascular risk with increasing degree of hyperglycemia. In a community-based sample of elderly patients hospitalized with acute MI from 1994 to 1996, higher glucose levels were associated with higher risk of 30-day mortality in patients without known diabetes (glucose ≤110 mg/dL; range from glucose >110 to 140 mg/dL: hazard ratio [HR] 1.17; 95% CI 1.11-1.24; to glucose ≥240 mg/dL: HR 1.87; 95% CI 1.75-2.00) [11]. (See "Prevalence of and risk factors for coronary heart disease in patients with diabetes mellitus", section on 'CHD before diabetes'.)

Outcomes after myocardial infarction — Outcomes after acute MI in patients with diabetes are worse than in patients without diabetes, particularly in women (figure 1) [12-14]. In the TIMI ACS trials from 1997 to 2006, 10,613 patients had diabetes (17 percent of the overall population). Diabetes was independently associated with higher mortality at 30 days after unstable angina/non-ST elevation MI (2.1 versus 1.1 percent; odds ratio [OR] 1.78; 95% CI 1.24-2.56) or STEMI (8.5 versus 5.4 percent; OR 1.40; 95% CI 1.24-1.57) [15].

Similar observations have been seen in other cohorts [4,12,13,16-18]. The reason for these associations are likely multifactorial and include higher burden of coronary artery disease, increased comorbidities such as renal disease, and increased acuity at the time of presentation.

In the TAMI trial, patients with diabetes were more likely to present in acute pulmonary edema than patients without diabetes (11 versus 4 percent in TAMI) [12]. The increased incidence of heart failure frequently occurs despite similar infarct sizes and left ventricular ejection fractions [12,13,19].

One or more of the following may contribute to the higher incidence of heart failure at the time of MI in diabetics:

A greater extent of coronary disease (ie, more multivessel disease) which affects myocardial performance by limiting blood flow to noninfarcted myocardium [12,20,21].

Intrinsic myocardial dysfunction. (See "Heart failure in patients with diabetes mellitus: Epidemiology, pathophysiology, and management".)

An increased incidence of prior MI [19,20].

Diabetic patients also may have a higher risk of other complications, including arrhythmias, cardiogenic shock, heart failure, renal failure, and recurrent MI [4,13,14,16,17].

REPERFUSION — Many patients with acute MI benefit from early reperfusion.

ST-elevation myocardial infarction — Immediate coronary reperfusion is, in the absence of a contraindication, recommended in all patients with an acute ST-elevation MI (STEMI). This is usually achieved by primary percutaneous coronary intervention (PCI) or fibrinolytic therapy. Primary PCI is the preferred method for reperfusion after an acute ST-elevation MI since it produces better outcomes than thrombolysis. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome" and "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy".)

Primary percutaneous coronary intervention — Patients with diabetes have better outcomes with primary PCI (percutaneous transluminal coronary angioplasty [PTCA] or stenting) than with fibrinolysis. The best data come from a meta-analysis of pooled patient data from 19 randomized trials that enrolled 6315 patients, 14 percent of whom had diabetes [22]. The following statistically significant findings were noted at 30 days:

Mortality was lower after primary PCI than fibrinolysis (6.6 versus 12.4 percent; unadjusted OR 0.49, 95% CI 0.31-0.79).

Death or recurrent MI was reduced after primary PCI (9.6 versus 17.1 percent; unadjusted OR 0.52; 95% CI 0.35-0.77).

Stroke was reduced after primary PCI (1.5 versus 3.7 percent; unadjusted OR 0.40; 95% CI 0.16-0.99).

The value of primary PCI with stenting compared to PTCA alone was evaluated in the CADILLAC trial in which 2082 patients with acute STEMI (almost 17 percent diabetic) were randomly assigned to PTCA alone, PTCA and abciximab, stenting alone, or stenting and abciximab; clopidogrel or ticlopidine was given to all patients initially and then continued in those who received a stent [23]. The outcomes were significantly better with stenting and the relative benefit was similar in patients with or without diabetes (OR 0.56 and 0.52, respectively). In the cohort with diabetes, the rate of target vessel revascularization at one year was higher in patients treated with PTCA when compared with coronary stenting (10.3 versus 22.4 percent, p = 0.004). There were no significant differences in the other endpoints including death, reinfarction, or stroke [24].

One possible contributor to the worse outcomes in diabetics is microvascular disease. This issue was addressed in a report of two substudies from the CADILLAC trial [25]. Two markers of tissue perfusion were evaluated: TIMI myocardial perfusion (blush) grade on angiography and ST segment resolution. (See "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction", section on 'Primary failure'.)

The following findings were noted:

Postprocedural TIMI flow grade 3 (normal flow) was attained in more than 95 percent of patients (including those with and without diabetes).

Patients with diabetes were significantly more likely to have a TIMI myocardial perfusion (or blush) grade of 0/1 after PCI (56 versus 47 percent in nondiabetics), indicating little or no tissue perfusion.

Patients with diabetes were significantly more likely to have persistent ST-segment elevation (20 versus 8 percent), indicating a larger area with endangered perfusion.

These persistent abnormalities were associated with a trend toward increased mortality in patients with diabetes. Similar findings in diabetics (reduced myocardial blush grade and impaired ST-segment resolution after primary PCI) have also been noted in other studies [26].

Fibrinolytic therapy — Patients with diabetes and ST-elevation myocardial infarction (STEMI) appear to derive the same or greater benefit (including mortality) from fibrinolytic therapy as patients without diabetes [27]. For patients who cannot receive timely PCI, fibrinolytic therapy should be considered.

While there has been a specific concern about the use of fibrinolytics with regard to the potential risk of intraocular hemorrhage in patients with diabetic retinopathy, we do not believe it is a major contraindication. Among 6011 patients with diabetes in the GUSTO-I trial, it was estimated that about 2000 had nonproliferative retinopathy and about 300 had proliferative retinopathy [28]. Only one patient had an ocular hemorrhage, which was an eyelid hematoma. Although the risk of ocular hemorrhage was not as completely evaluated in other major thrombolytic trials, an appreciable number of diabetics were included without reports of major intraocular bleeding [29].

Non-ST-elevation myocardial infarction — In patients with an acute NSTEMI, an early invasive strategy in which patients go for coronary angiography with plans to proceed with revascularization (if amenable) within 48 hours of the index event has been shown to reduce cardiovascular events [30]. This benefit appears proportional to the risk of the patient. Given the increased risk associated with diabetes, this cohort warrants an early invasive strategy when presenting with NSTEMI. Coronary angiography, performed in the acute period following NSTEMI, demonstrates that the infarct-related artery is not occluded in 60 to 85 percent of cases.

However, because of improved long-term outcomes with revascularization, almost all patients with a NSTEMI are candidates for early angiography (performed within 4 to 48 hours after presentation) followed by revascularization with either percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG) if appropriate. Given the higher prevalence of multivessel coronary artery disease in patients with diabetes, they are more likely to need CABG [31]. This topic will not be discussed further here since the presence or absence of diabetes does not influence decision making other than denoting the cohort of patients with diabetes as high risk in nature. (See "Coronary artery revascularization in stable patients with diabetes mellitus".)

ANTICOAGULANT THERAPY — Early anticoagulation remains a cornerstone of treatment for patients hospitalized with acute MI. The choice of anticoagulants is similar irrespective of the presence or absence of diabetes. Intravenous heparin is the preferred agent in patients undergoing PCI [32]. (See "Acute ST-elevation myocardial infarction: Management of anticoagulation" and "Anticoagulant therapy in non-ST elevation acute coronary syndromes".)

ANTIPLATELET THERAPY — All MI patients, including those with diabetes, should receive aspirin (see "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease", section on 'Summary and recommendations') and a P2Y12 receptor blocker as soon as possible after the diagnosis has been made. The choice of the P2Y12 receptor blocker depends on the reperfusion strategy. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Our approach to early DAPT'.)

In every major trial which compared clopidogrel to placebo or prasugrel or ticagrelor to clopidogrel, outcomes in the subgroup of patients with diabetes were similar to the broad population of patients enrolled [33-38].

Patients with diabetes mellitus have increased platelet reactivity, with intensified adhesion, activation, and aggregation. This appears to be due to dysregulation of several signaling pathways secondary to changes at the receptor level (eg, increased expression) and abnormalities in intracellular downstream signaling [39,40]. These abnormalities may partially explain the higher risk of developing an acute coronary syndrome, as well as in the larger proportion of diabetes patients with inadequate response to antiplatelet agents (eg, clopidogrel, aspirin) compared to patients without diabetes. (See "Clopidogrel resistance and clopidogrel treatment failure", section on 'Diabetes mellitus'.)

Since clopidogrel is a pro-drug that may be metabolized into its active form via the liver, there is patient-level variation in platelet reactivity [39,40]. Patients with diabetes are more likely to have high platelet reactivity during treatment with clopidogrel. These patients are at increased risk of major adverse cardiovascular events [41]. Patients with diabetes benefit from more intensive antiplatelet therapy, and we choose ticagrelor in most cases. (See "Clopidogrel resistance and clopidogrel treatment failure", section on 'Diabetes mellitus'.)

Intravenous glycoprotein IIb/IIIa inhibitors — For patients with diabetes and MI who receive early antiplatelet therapy with aspirin and a P2Y12 inhibitor, we recommend not routinely using a GP IIb/IIIa inhibitor. In those patients undergoing PCI who have not been treated with a P2Y12 inhibitor, intravenous cangrelor can be considered. GP IIb/IIIa inhibitor should be reserved for patients with thrombotic complications of PCI. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Intravenous agents'.)

SECONDARY PREVENTION — Similar to the broad group of patients with acute MI, we employ multiple secondary preventive interventions in those with diabetes. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

Lipid lowering — Patients with diabetes mellitus are considered to be at very high risk for subsequent coronary artery disease events. Aggressive low density lipoprotein cholesterol (LDL-C) lowering is beneficial in all patients with a prior MI. Patients should be started on high-intensity lipid-lowering therapy, such as with atorvastatin 80 mg daily, while in the hospital. (See "Low-density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome".)

Beta blockers — Beta blocker therapy after MI reduces infarct size, the incidence of infarct extension, recurrent ischemia, reinfarction, and cardiac and sudden death mortality. The concern about the possibility of masking hypoglycemic symptoms or worsening glycemic control has made some physicians reluctant to prescribe beta blockers to patients with diabetes. However, these concerns have been overstated, and analysis of outcomes of diabetic subgroups in several postinfarction beta blocker trials has shown an overall benefit from the use of beta blockers that is at least equivalent to and may be greater than that seen in patients without diabetes [42,43]. (See "Acute myocardial infarction: Role of beta blocker therapy".)

The National Cooperative Cardiovascular Project reviewed the records of 45,308 patients 65 years of age or older, 26 percent of whom had diabetes [44]. After adjusting for potential confounders, use of beta blockers was associated with a lower one-year mortality rate for patients with both insulin and non-insulin-treated diabetes. The association between use of beta blockers and outcomes was similar to that seen in patients without diabetes. There was no association with an increased risk of readmission for diabetes-related complications. Despite these data, patients with diabetes were less likely to receive beta blockers when compared with patients without diabetes.

ACE inhibitors — All patients with diabetes should be considered for an angiotensin converting enzyme (ACE) inhibitor or, if not tolerated, an angiotensin II receptor blocker early after the diagnosis of an MI. When given after an acute MI, ACE inhibitors reduce infarct size, limit ventricular remodeling, and reduce mortality.

They may be of particular benefit in patients with diabetes. Many patients with type 1 and 2 diabetes will be treated with an ACE inhibitor or angiotensin II receptor blocker for blood pressure control and risk mitigation even before their myocardial event. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use" and "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Clinical trials", section on 'Effects in all patients'.)

The GISSI-3 trial of patients with acute MI, which included 2790 patients with diabetes, found that six weeks of treatment with lisinopril reduced mortality (odds ratio 0.88; 95% CI 0.79-0.99) [45]. In the cohort with diabetes, six-month mortality was reduced (12.9 versus 16.1 percent) (figure 2) [46]. The benefit of ACE inhibition translated into 37 lives saved per 1000 treated patients, an effect that was higher than that observed in patients without diabetes.

Aldosterone antagonists — We recommend an aldosterone receptor blocker to all patients with diabetes who meet the following criteria, which were derived from the EPHESUS trial of patients 3 to 14 days after acute MI [47,48]:

Are receiving an ACE inhibitor and a beta blocker

Have a left ventricular ejection fraction ≤40 percent

Have a serum creatinine ≤2.5 mg/dL (221 micromol/L) in men and ≤2.0 mg/dL (177 micromol/L) in women

Have a serum potassium ≤5.0 mEq/L

The serum potassium must be monitored closely during treatment. Although uncommon, life-threatening hyperkalemia can occur due to the combination of aldosterone inhibition and reduced aldosterone secretion associated with ACE inhibitor therapy, and, in some patients, renal insufficiency. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Mineralocorticoid receptor antagonist'.)

Glycemic control — The optimal target range of blood glucose in patients with acute MI is uncertain. In patients with acute MI who are critically ill (eg, receiving care in an intensive care unit), it is reasonable to use target blood glucose values appropriate for patients with critical illness; these target values are described elsewhere. (See "Glycemic control in critically ill adult and pediatric patients", section on 'Target range of blood glucose'.)

Patients with acute MI who are not critically ill should be treated for hyperglycemia according to standards for hospitalized patients, which are discussed separately. (See "Management of diabetes mellitus in hospitalized patients", section on 'Noncritically ill'.)

A number of trials addressed the effects of intensive insulin therapy or glycemic control in patients with acute MI, but they arrived at different conclusions and had flaws that limit their generalizability to practice [49-51].

Other drugs

Sodium glucose-like co-transporter-2 inhibitors — Sodium glucose-like co-transporter-2 (SGLT2) inhibitors including empagliflozin, canagliflozin and dapagliflozin reduce cardiovascular events by approximately 15 percent, largely in patients with prior cardiovascular events. The role of SGLT2 inhibitors in patients with diabetes is discussed elsewhere. (See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Patient selection' and "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Cardiovascular effects'.)

SGLT2 inhibitors should be utilized in patients with diabetes following a myocardial infarction. There are no data available to support use during the acute event. Thus, these agents should be considered once patients are stabilized from their acute event, particularly in those patients in whom the risk of heart failure is elevated.

GLP-1 receptor agonists — Randomized clinical trials to establish cardiovascular safety have found that some glucagon-like peptide 1 receptor (GLP-1) agonists decrease cardiovascular events in patients with diabetes (see "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus"). In a meta-analysis of seven trials, GLP-1 receptor agonists reduced cardiovascular death, MI, or stroke in patients with established coronary artery disease by 14 percent (HR 0.86, 95% CI 0.79-0.94). However, there are differences across the class with regard to the effects of an agent on cardiovascular events. GLP-1 receptor agonists have been shown to decrease cardiovascular events in the cohort of patients with established cardiovascular disease [52]. Similar to SGL2i, these agents should be considered once patients are stabilized from their acute event.

Metformin — While metformin is first-line therapy for patients with diabetes, there have been no adequately powered randomized clinical trials to assess its benefit following an MI. In the GIPS III trial, there was no difference in left ventricular function at four months [53].

Regulators of gene transcription — Small molecule regulators of gene transcription, such as bromodomain and extraterminal (BET) proteins, may be involved in the pathogenesis of atherosclerosis (see "Pathogenesis of atherosclerosis", section on 'Pathogenesis'). The ability of apabetalone, a selective inhibitor of these proteins, to improve cardiovascular outcomes after ACS has been evaluated. In the BETonMACE randomized trial of 2425 ACS patients with diabetes and low high-density lipoprotein cholesterol, apabetalone did not significantly lower the rate of a composite of adverse cardiovascular outcomes during more than two years of follow-up (hazard ratio 0.82, 95% CI 0.645-1.04) [54].

Blood pressure control — Hypertension should be aggressively treated in patients who have diabetes mellitus. The optimal goal blood pressure and choice of antihypertensive drugs in such patients are discussed in detail separately. (See "Treatment of hypertension in patients with diabetes mellitus".)

Multifactorial risk factor reduction — The benefits associated with multifactorial risk factor reduction (eg, aspirin, blood pressure and glycemic control, and cessation of smoking) in patients with diabetes have been demonstrated in multiple studies [55,56]. Cardiac rehabilitation is indicated for patients with ACS and can be helpful in initiating lifestyle changes. The details of the protocol and overall results of this study are discussed elsewhere. (See "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Multifactorial risk factor reduction' and "Cardiac rehabilitation: Indications, efficacy, and safety in patients with coronary heart disease", section on 'Summary and recommendations'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

SUMMARY AND RECOMMENDATIONS

Coronary heart disease patients with diabetes have worse long-term survival than those without diabetes. (See 'Introduction' above.)

The treatment of myocardial infarction (MI) in patients with diabetes mellitus is largely similar to that in those without diabetes.

Patients with acute coronary syndrome (ACS) and diabetes should undergo early reperfusion. (See 'Reperfusion' above.)

In patients with ST-elevation MI (STEMI), immediate percutaneous coronary intervention (PCI) is recommended. (See 'ST-elevation myocardial infarction' above.)

In patients with NSTE-ACS, an early invasive strategy is recommended. The mode of revascularization, PCI or coronary artery bypass graft surgery, is dependent upon clinical variables including severity/burden of disease, anatomy, and patient characteristics. (See 'Non-ST-elevation myocardial infarction' above.)

Following ACS, patients should be treated with aggressive secondary prevention strategies. (See 'Secondary prevention' above.)

This includes (but is not limited to) aspirin, high-dose statin therapy, beta blockers, renin-angiotensin-aldosterone system inhibitors, sodium-glucose co-transporter 2 inhibitors, and glucagon-like peptide-1 agonists in appropriate patients.

The optimal target range of blood glucose in patients with acute MI is uncertain. In patients with acute MI who are critically ill (eg, receiving care in an intensive care unit), it is reasonable to use target blood glucose values appropriate for patients with critical illness. These targets are described elsewhere. (See "Glycemic control in critically ill adult and pediatric patients", section on 'Target range of blood glucose'.)

Patients with acute MI who are not critically ill should be treated for hyperglycemia, if present, according to standards for hospitalized patients, which are discussed separately. (See "Management of diabetes mellitus in hospitalized patients", section on 'Noncritically ill'.)

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Topic 84 Version 32.0

References

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