Silent Ischemia: Current Concepts and Management

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Group A consisted of nine patients with reproducible stress-induced angina; group B consisted of nine patients with reproducible stress-induced myocardial ischemia but no angina. Positron emission tomography was used to measure regional cerebral blood flow changes as an index of neuronal activation during painful and silent myocardial ischemia induced by intravenous dobutamine.

Regional cerebral blood flow changes during myocardial ischemia were compared with those during baseline conditions and during placebo infusion. During myocardial ischemia, regional cerebral blood flow increased bilaterally in the thalami and prefrontal, basal frontal, and ventral cingulate cortices in patients in group A. Both thalami were activated in group B, but cortical activation was limited to the right frontal region. In both groups, thalamic regional cerebral blood flow remained increased after the symptoms and signs of ischemia had ceased.

Bilateral activation of the thalamus can be shown in both angina and silent ischemia; thus, peripheral nerve dysfunction cannot completely explain silent ischemia. Frontal cortical activation appears to be necessary for the sensation of pain. Abnormal central processing of afferent pain messages from the heart may play a determining role in silent myocardial ischemia.

Ann Intern Med.

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Cardiology , Coronary Heart Disease. Results provided by:. Sign In Set Up Account. You will be directed to acponline. Open Athens Shibboleth Log In. Subscribe to Annals of Internal Medicine. Advanced Search. Original Research 1 June Acknowledgments: The authors thank Mr. Ignathios Ikonomides for assistance with echocardiography; and Professor Alberto Malliani, Universita di Milano, for helpful advice. Requests for Reprints: Dr. Current Author Addresses: Drs. Abstract Objective: To test whether the silence of painless myocardial ischemia is caused by abnormal handling by the central nervous system of afferent messages from the heart.

Design: Nonrandomized study. Setting: A tertiary referral center postgraduate medical school. Patients: 2 matched groups of nondiabetic patients with coronary artery disease.

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Measurements: Positron emission tomography was used to measure regional cerebral blood flow changes as an index of neuronal activation during painful and silent myocardial ischemia induced by intravenous dobutamine. Results: Regional cerebral blood flow changes during myocardial ischemia were compared with those during baseline conditions and during placebo infusion. Conclusions: Bilateral activation of the thalamus can be shown in both angina and silent ischemia; thus, peripheral nerve dysfunction cannot completely explain silent ischemia. Nifedipine had no significant effect on either measured variable for ambulatory ischemia.

Frequency of angina was significantly decreased by both propranolol and diltiazem. Despite these limitations, the study first demonstrated a role for beta-blocker and calcium channel blocker therapy to reduce frequency and duration of silent ischemia in the stable angina population. Subsequently, atenolol was studied versus nifedipine in 24 patients with stable exertional angina and transient silent ischemia during ambulatory electrocardiography. Both atenolol and nifedipine were effective in reducing the average number and duration of transient ischemic events.

In addition, the atenolol group had a significant decrease in duration of early morning silent ischemia. The ASIST trial demonstrated that atenolol treatment reduced daily ischemia and was associated with reduced risk for adverse outcome in asymptomatic and mildly symptomatic patients compared with the placebo.

Other beta-blockers, such as bisoprolol, have been studied, as in Total Ischemic Burden Bisoprolol Study TIBBS , which was an 8-week randomized comparison of bisoprolol and nifedipine on transient ischemic episodes in patients with stable angina. The TIBBS trial demonstrated a correlation between the number of episodes and event rates, as well as a greater reduction of ischemia with bisoprolol than nifedipine followed by an improved outcome at 1 year The Asymptomatic Cardiac Ischemia Pilot Study ACIP also evaluated beta-blockers and calcium channel blockers in combination with other pharmacologic agents in comparison with myocardial revascularization as discussed below.

The pharmacologic treatment aims for an angina-guided strategy and for an ischemia-guided strategy, including atenolol plus nifedipine if needed, versus diltiazem plus isosorbide dinitrate if needed. Both strategies were effective in reducing the number of episodes and total duration of ischemia on ambulatory electrocardiography, which further supports earlier work regarding the efficacy of these pharmacologic agents in an asymptomatic cardiac ischemia population with both short-term ischemia suppression and long-term improvement in outcomes out to 2 years.

Follow-up of outcomes to 1 year in ACIP reaffirmed that the revascularization group received less medication and had less ischemia on serial ambulatory ECT recordings and exercise testing than those assigned to medical strategies. Despite the relatively small sample size, the mortality rates at 1 year were 4. Therefore, revascularization better suppressed asymptomatic ischemia and was associated with better outcome at 1 year.

It is important to note that this trial was performed prior to the advent of PCI with stenting, which is a limitation for modern day applicability. At 2 years, the ACIP trial, these data were reaffirmed as the initial revascularization strategy improved prognosis of the population compared with the angina-guided pharmacologic therapy.

Current Concepts and Management

The intensity of the pharmacologic therapy was also an issue compared with modern day optimal medical therapy. The study revealed a persistent benefit of revascularization with PTCA compared with antiischemic pharmacologic therapy, including secondary preventive measures for the long-term outcome of asymptomatic patients with silent ischemia post MI.

There was a significant reduction in long-term mortality out to Follow-up from this trial population has demonstrated that the rate of sudden cardiac death SCD corresponded to an average annual event rate of 0. These findings have confirmed earlier data, once again reinforcing the importance of silent myocardial ischemia from a prognostic standpoint and reaffirming the increased risk of hard endpoints such as sudden cardiac death SCD.

More recently, the common practice of using stress myocardial perfusion scintigraphy MPS to identify ischemia in patients with prior revascularization in the era of contemporary optimal medical therapy was studied in patients who had asymptomatic ischemia from to and followed for a median of 5. The analysis was performed with development of a propensity score to express the associations of revascularization.

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After adjusting for baseline characteristics, type of prior revascularization, MPS data and propensity scores, only age and hypercholesterolemia but not revascularization were associated with mortality. Therefore, asymptomatic patients with history of revascularization and inducible ischemia on MPS had no significant benefit from repeat revascularization and an ischemia-based strategy did not alter mortality or improve survival compared with medical therapy.

These data suggest that intensive pharmacologic therapy from contemporary trials likely impact the net benefit when comparing medical therapy with revascularization. Unlike earlier studies, this analysis also uses modern percutaneous coronary intervention with use of drug eluting stent technology and therefore closely reflects current clinical practice. Although prior studies have evaluated the symptomatic population with ischemia post-revascularization, which is supported by literature and clinically appropriate, the current study raises an important point in the asymptomatic post-revascularization subgroup with ischemia.

The COURAGE trial demonstrated that a strategy of initial revascularization with optimal medical therapy had no survival benefit over optimal medical therapy alone in patients with stable ischemic heart disease and angiographically documented CAD. The event rates were not significantly increased with OMT alone and these data were discordant with earlier studies, demonstrating that the extent of ischemia was associated with greater benefit in all-cause mortality, with early revascularization compared with optimal medical therapy in earlier trials.

Use of a different stress modality in stress echocardiography did not show a survival benefit with repeat revascularization in the asymptomatic population. A recent post hoc analysis of the COURAGE Trial evaluated clinical outcomes in patients with silent myocardial ischemia as compared to those with symptomatic ischemia during a 5-year follow-up. When compared to the symptomatic patients, there were no major differences in baseline clinical characteristics nor were there differences in death or MI as compared with symptomatic patients.

There were, however, significantly fewer hospitalizations for ACS and a lower rate of subsequent revascularization in the patients with silent ischemia. When outcomes were compared as a function of treatment strategy, there were no overall differences among the silent ischemia patients between those randomized to PCI or medical therapy for the endpoints of death or MI. While these data should be interpreted as hypothesis-generating, they do suggest that myocardial revascularization may play a potential role in improving prognosis in these patients.

It is well established that coronary artery disease CAD is a major complication of diabetes mellitus and CAD is leading cause of death in patients with type II diabetes mellitus.


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The risk is validated and guidelines have deemed type 2 diabetes as a coronary artery disease risk equivalent. The issue of SMI and DM has been studied in the Detection of Ischemia in Asymptomatic Diabetics DIAD randomized controlled trial in which patients were randomly assigned either to be systematically screened with stress myocardial perfusion imaging MPI or not to be screened with the hypothesis that systematic screening would identify higher risk individuals and beneficially affect their risk of myocardial infarction or death.

Some 1, patients, aged 50 to 75 years with type II DM were enrolled with no known or suspected CAD, and the prevalence of ischemia was assessed by adenosine tehnetiumm sestamibi single-photon emission computed tomography myocardial perfusion imaging. The strongest predictors for abnormal tests were abnormal Valsalva HR 5. However, in follow-up mean 4.

Seven nonfatal MIs and 8 cardiac deaths 2. The overall rate of coronary revascularization was low in both groups with 31 5. The outcomes study concluded that in the contemporary population of patients with diabetes, the cardiac event rates were low and were not significantly reduced by MPI screening for myocardial ischemia over 4. Diabetic patients continue to pose a challenging clinical scenario as to how best to screen the asymptomatic high-risk patient for silent ischemia and whether there is any clinical benefit compared with standard control of cardiovascular risk factors.

The study included male and female patients with diabetes aged The main study endpoint was time to death from all causes, nonfatal myocardial infarction, nonfatal stroke, or heart failure requiring hospitalization or emergency service intervention. The study was discontinued prematurely because of difficulties in recruitment and a lower than expected event rate. Follow-up was complete for Silent ischemia detection was positive or uncertain in 68 There was no significant difference between the screening and the usual care group for the main outcome HR 1.

A meta-analysis combining these data and the DIAD data gave similar results, with narrow confidence intervals for each endpoint, and suggesting overall that the systematic detection of silent ischemia in high-risk asymptomatic patients with diabetes is unlikely to provide any major benefit on hard outcomes in patients whose cardiovascular risk is controlled by optimal medical treatment.

In diabetic patients, with a defective anginal warning system, it is reasonable to assume that asymptomatic ischemia has a prognostic significance similar to that of symptomatic ischemia and that their management with respect to disease-modifying preventive therapy, coronary angiography, and revascularization should be similar.


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Although suppression of ischemia in patients with asymptomatic ischemia appears to be a worthwhile objective, whether treatment should be guided by symptoms or by ischemia as reflected by the ambulatory ECG has not been established. Nevertheless, it seems reasonable to use antiischemic pharmacologic therapy in patients with well-documented myocardial ischemia, even if symptoms are lacking. Aggressive secondary prevention with lipid-lowering therapy has also been shown to reduce ischemia on ambulatory monitoring. Cohn, P. Am J Cardiol. Seminal early work outlining the concept of silent ischemia and the potential of a defective angina warning.

Am J Med. Landmark study quantifying the degree of silent ischemia in patients with and without angina symptomatology. Fleg, JL.

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Critical original work in healthy subjects with early study of exercise-induced silent ischemia. Deedwania, P, Carbajal, E. Landmark study describing patients with stable angina on pharmacologic antianginal therapy. Koistinen, MJ. Seminal study of the prevalence of silent ischemia in the diabetic population.

Landmark trial to further study the detection of silent ischemia in diabetics.

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J Am Coll Cardiol. Contemporary review article summarizing 3 decades of research in silent ischemia. Differential effects on ambulatory ischemia, exercise performance, anginal symptoms. N Engl J Med.