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8.1. Psychosocial Impact of STEMI

Class I

The psychosocial status of the patient should be eval- uated, including inquiries regarding symptoms of depression, anxiety, or sleep disorders and the social

support environment. (Level of Evidence: C)

Class IIa

Treatment with cognitive-behavioral therapy and selective serotonin reuptake inhibitors can be useful for STEMI patients with depression that occurs in the

year after hospital discharge. (Level of Evidence: A)

Depression is a common consequence of STEMI, with major depression occurring in 15% to 20% of patients with STEMI and some degree of clinically significant depression occurring in up to half (1339). Most studies have found depression to be a significant independent predictor of post- MI mortality (1340-1345), although others have not (1346,1347). An ancillary follow-up study from the ENRICHD trial (Enhancing Recovery in Coronary Heart Disease) of a subsample of 358 depressed patients with an acute MI compared with 408 nondepressed patients found that the depressed patients were at higher risk for all-cause mortality but not until nearly 12 months after the acute event. Depression did not predict nonfatal recurrent infarction (1348). The excess risk associated with depression soon after STEMI remains significant for a longer time than previously thought, and a dose-response relationship exists between depression and mortality. The level of depression symptoms at the time of STEMI admission is more closely linked to long-term (5-year) survival than the level at 1 year, notably so in patients with moderate to severe levels of depression. Even minimal degrees of depression appear to confer risk, and risk increases with degree of depression as measured on the Beck Depression Inventory (1340). Depression markedly decreases quality of life for post-STEMI patients (1339,1346,1347,1349,1350) and is associated with substan- tially greater costs (1341). Fatigue does not explain the impact of STEMI in producing depression (1343), nor do infarct size, LV function, or other physiological variables predict the degree of depression (1345,1339). Depression rather than physiological variables predicts failure to return to usual activity and failure of social role resumption after MI (1351). Depressed patients are less likely to complete

7.12.13. Antioxidants

Class III

Antioxidant vitamins such as vitamin E and/or vita- min C supplements should not be prescribed to patients recovering from STEMI to prevent cardio-

vascular disease. (Level of Evidence: A)

Earlier observational data from epidemiological studies suggested that an increased intake of lipid-soluble antioxi- dant vitamins (vitamin E and beta-carotene) is associated with reduced rates of cardiovascular events, including STEMI (1326-1328). In support of these data, one random- ized placebo-control study of vitamin E treatment in 2002 patients with documented coronary disease indicated a reduction in nonfatal MI (27% ARD; 77% RRR) but no effect on cardiovascular death or overall mortality (1329). However, a midstudy change in the vitamin E dose and some imbalance in the use of beta-adrenoceptor blockers in sub- jects receiving vitamin E make interpretation of that study problematic. A prospective cohort study of more than 34 000 postmenopausal women suggested that an increase in dietary vitamin E but not supplemental vitamin E was associated with decreased cardiovascular risk (1330). In a randomized trial involving 11 324 patients surviving recent (less than 3 months) MI, patients were assigned to treatment with the fol- lowing: vitamin E (300 mg daily; n equals 2830); n-3 polyunsaturated fatty acids (1 g daily; n equals 2836); both (n equals 2830); or neither (n equals 2828) for 3.5 years. Treatment with n-3 polyunsaturated fatty acids but not vita- min E significantly lowered the relative risk of the primary end point (death, nonfatal MI, or stroke) by 10% (p equals 0.048) (1331). Thus, although dietary supplementation with n-3 polyunsaturated fatty acids may have clinical benefits for patients after STEMI, this trial failed to demonstrate a treat- ment benefit for vitamin E. With regard to beta-carotene, several prospective studies have convincingly shown a lack of beneficial effect on cardiovascular disease (1332-1334), and 2 studies have indicated an increase in lung cancer with beta-carotene treatment (1332,1333).

There is even less evidence to support the use of water-sol- uble enzymatic antioxidants for cardiovascular disease. Although one study suggested reduced cardiovascular risk in subjects taking supplemental vitamin C (1335), the majority of other large epidemiological studies have not indicated a benefit (1326-1328). Thus, routine use of vitamin C after STEMI cannot be recommended.

Despite promising experimental studies, recombinant superoxide dismutase failed to reduce infarct size in a well- controlled primary PCI trial (1336). One small study showed a trend for reduced restenosis with vitamin E treatment after coronary angioplasty (restenosis rate 35.5% for treatment group versus 47.5% for placebo group; n equals 100, p equals 0.06) (1337). A larger study evaluating the combina- tion of vitamin E in association with omega-3 fatty acids 2 weeks before elective PCI showed no effect on the resteno- sis rate (1338).

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cardiac rehabilitation and less likely to adhere to important lifestyle changes and medications. (1352,1353).

Treatment of depression with combined cognitive-behav- ioral therapy and selective serotonin reuptake inhibitors improves outcome in terms of depression symptoms and social function (1350,1354,1355). A double-blind study comparing sertraline and placebo found that sertraline was associated with clinically meaningful improvement in multi- ple quality-of-life domains in patients hospitalized with acute coronary syndrome (74% of which was acute MI) in the previous month who had recurrent depression (1350). Although one randomized controlled trial showed no reduc- tion in mortality or reinfarction (1355), a reanalysis suggest- ed its follow-up was not long enough to demonstrate effect, and indeed, depression was associated with mortality in that study (1348). Therefore, it appears prudent to assess patients with STEMI for depression during hospitalization and during the first month after STEMI and to intervene and reassess yearly in the first 5 years, as appropriate. There is evidence that the STEMI experience, with its sudden and unexpected onset, dramatic changes in lifestyle, and the additive effort of comorbid life events, is a relatively traumatic event and may produce impaired coping during subsequent ischemic events (1356).

Social integration and social support repeatedly have been shown to influence outcomes after STEMI. Social integra- tion refers to the existence of social ties (e.g., spouse, close family members, or friends) and degree of participation in group activities (e.g., family gatherings, religious affilia- tions). Social support refers to the actual or perceived receipt of information, materials, and/or emotional support.

Mortality from all causes, including ischemic heart disease, is lower in socially integrated individuals (1357). Recurrent cardiac events are also significantly lower among persons reporting high levels of social integration than among social- ly isolated persons (1358,1359). When social support was clearly defined and measured and the effect of depression was controlled for, a large prospective trial (1360) demon- strated that support did not directly predict post-MI mortali- ty. However, high levels of support mitigated the effect of depression on post-MI mortality. A randomized controlled trial of a social support and depression management inter- vention similarly did not demonstrate reduced mortality (1355) but did significantly reduce social isolation.

The most effective social support interventions occur natu- rally. The quality of the support provided is key; support has been shown to facilitate treatment compliance, but only when policing is minimized (1362). Overprotectiveness and withholding of information or worries, either of the patient by family members or vice versa, is associated with worse outcomes (1363,1364). Telephone follow-up, cardiac reha- bilitation, or other group events can be effective methods of support for socially isolated individuals (1365).

Anxiety is prevalent among hospitalized patients with STEMI but declines relatively rapidly after discharge to lev- els typical of the general medical population (1366). Anxiety is predictive of in-hospital recurrent ischemia and arrhyth-

mias after MI (707), and physicians’ and nurses’ subjective judgments of patient anxiety are not accurate compared with measurement on validated scales (709). At least one random- ized controlled trial demonstrates that in-hospital anxiety and depression can be reduced by a structured nursing support intervention (714), and secondary analysis of a longer-term trial suggests that both long-term psychosocial distress and health outcomes may benefit (1367). Anxiety should be assessed at the time of hospital discharge of patients hospi- talized for STEMI. A number of studies have examined psy- chological intervention programs designed to help post-MI patients’ psychosocial and emotional adjustment. Two large post-MI programs (1341,1368) failed to achieve positive outcomes on psychological factors or prognosis. Some have observed that the type of approach used with patients recov- ering from MI varies in terms of its association with anxiety reduction (1367,1369). Nevertheless, one meta-analysis reported that the addition of psychosocial interventions to standard treatment resulted in significantly less depression, anxiety, morbidity, and mortality (1370). Psychosocial inter- ventions in cardiac rehabilitation were found in another review to improve the odds for mortality and recurrence of nonfatal MI, but not necessarily with regard to females and older participants (1369). A secondary analysis of a longer- term trial suggests that both long-term psychosocial progno- sis and health outcomes may improve in patients whose psy- chological status improves (1367).

8.2. Cardiac Rehabilitation

Class I

Cardiac rehabilitation/secondary prevention pro- grams, when available, are recommended for patients with STEMI, particularly those with multiple modifi- able risk factors and/or those moderate- to high-risk patients in whom supervised exercise training is war-

ranted. (Level of Evidence: C)

Cardiac rehabilitation programs are designed to limit the physiological and psychological effects of cardiac illness, reduce the risk for sudden death or reinfarction, control car- diac symptoms, stabilize or reverse the atherosclerotic process, and enhance the psychosocial and vocational status of selected patients (1184,1371,1372). Cardiac rehabilitation is a comprehensive long-term program that involves medical evaluation, prescribed exercise, cardiac risk factor modifica- tion, education, and counseling (1184,1373). Cardiac reha- bilitation can occur in a variety of settings, including super- vised groups in a hospital, physician’s office, or community facility. In clinically stable lower-risk patients, rehabilitation can be undertaken independently, with regular guidance from a cardiac rehabilitation healthcare professional (1184). The exercise can be supervised or unsupervised and can involve a stationary bicycle, treadmill, calisthenics, walking, or jog- ging. Home exercise training programs have been shown to be beneficial in certain low-risk patient groups. They offer

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frequently to cardiac rehabilitation programs, even though they have been reported to derive benefit (1378-1380).

8.3. Follow-Up Visit With Medical Provider

Class I

1. A follow-up visit should delineate the presence or