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Silent ischemia: Tip of the iceberg
Silent lschemia Tip of the Iceberg WILLIAM
W. PARMLEY, M.D.
ost physicians have, over the years, become comfortable with the diagnosis of angina pectoris and the management of patients with coronary artery disease. Therapy is centered on relieving discomfort in the chest by reducing the myocardial oxygen demand/supply ratio with a variety of drugs or interventions. Since angina can be reduced by such therapy, a ready marker of treatment efficacy is available that satisfies both patients and physicians alike. With the increasing recognition of the prevalence of silent ischemia, however, uncertainty exists about the need for detection, the prognostic implications, and the approach to therapy. In asymptomatic patients, it seems intuitive that no therapy employed can make them feel better. The question is, however, will it help them to live longer? This supplement issue explores some of the thorny issues related to the syndrome of silent ischemia. It appears that there is increasing interest in this entity, and that much more information will be forthcoming in the future. The contributors to this issue have had considerable research experience with silent myocardial ischemia. Each article examines a different facet of the problem, leading to a well-rounded summary of a fascinating clinical syndrome. Cohn points out in his article that about four to five million patients in the United States have silent ischemia, including 50,000 asymptomatic patients who have had myocardial infarction. Data suggest that the prognosis,for these patients varies with the extent of the coronary vessel involvement. Furthermore, Cohn links silent ischemia to sudden death. His provocative article will certainly offer future investigators and clinicians the challenge of devising strategies to identify patients at risk for sudden death due to silent ischemia. Deanfield et al review the use of ambulatory ST-segment monitoring as an objective technique for quantitating the frequency of silent ischemic episodes during daily life. Their article-notes that transient ischemia is more frequent and prolonged than is suggested by an analysis of chest discomfort alone. Positron emission tomography confirms that these episodes represent ischemia. Furthermore, the
M
majority of these episodes are unaccompanied by an increased heart rate, suggesting that an increased myocardial demand for oxygen does not play an important pathophysiologic role. Maseri et al discuss potential reasons why ischemia is silent in some patients and produces symptoms in others. The severity and duration of ischemia, neurophysiologic and psychologic differences between patients, and differences in pain thresholds all appear to be implicated. Miller describes the spectrum of silent ischemia in a variety of coronary artery disease syndromes, emphazing the role of vasoconstriction. Resnekov explores the potential roles of vasoconstriction, intramyocardial coronary arteries, and platelet aggregation. Various trigger mechanisms for silent ischemia are discussed, along with their clinical implications. Selwyn et al examine several clinical problems associated with silent ischemia. They raise important questions regarding the pathophysiology and prognostic implications of the frequent and sometimes prolonged episodes of silent ischemia in patients with coronary artery disease. Although numerous data are presented in this issue, it should be clear to readers that many questions remain unanswered. Should silent ischemia be actively looked for in groups of selected asymptomatic patients? Which patients are at high risk? Should high-risk patients be treated, and if so, how? In patients with angina and silent ischemia, it is tempting to try to minimize both phenomena. Certainly ischemia is an important adverse factor in all coronary syndromes in which it has been studied. Since silent ischemia occurs because of both an increased myocardial oxygen demand and a decreased supply, it may be important to select therapy that will affect both factors. Treatment with either calcium channel blockers, such as nifedipine, or nitrates, combined with beta blockers, may provide optimal anti-ischemic therapy. These and other questions will undoubtedly continue to challenge physicians for many years to come. It appears that careful therapeutic trials will ultimately be required to help clinicians decide how to best manage patients with silent ischemia.
From the University of California, San Francisco, School of Medicine, and the MoffittiLong Hospitals, Francisco, California. Requests for reprints should be addressed to Dr. William W. Parmley, Room Moffitt Hospital, University of California, 505 Parnassus Avenue, San Francisco, California 94143.
September
13, 1985
The American
Journal
of Medicine
Volume
San 1186,
79 (suppl
3A)
W. PARMLEY, M.D.
ost physicians have, over the years, become comfortable with the diagnosis of angina pectoris and the management of patients with coronary artery disease. Therapy is centered on relieving discomfort in the chest by reducing the myocardial oxygen demand/supply ratio with a variety of drugs or interventions. Since angina can be reduced by such therapy, a ready marker of treatment efficacy is available that satisfies both patients and physicians alike. With the increasing recognition of the prevalence of silent ischemia, however, uncertainty exists about the need for detection, the prognostic implications, and the approach to therapy. In asymptomatic patients, it seems intuitive that no therapy employed can make them feel better. The question is, however, will it help them to live longer? This supplement issue explores some of the thorny issues related to the syndrome of silent ischemia. It appears that there is increasing interest in this entity, and that much more information will be forthcoming in the future. The contributors to this issue have had considerable research experience with silent myocardial ischemia. Each article examines a different facet of the problem, leading to a well-rounded summary of a fascinating clinical syndrome. Cohn points out in his article that about four to five million patients in the United States have silent ischemia, including 50,000 asymptomatic patients who have had myocardial infarction. Data suggest that the prognosis,for these patients varies with the extent of the coronary vessel involvement. Furthermore, Cohn links silent ischemia to sudden death. His provocative article will certainly offer future investigators and clinicians the challenge of devising strategies to identify patients at risk for sudden death due to silent ischemia. Deanfield et al review the use of ambulatory ST-segment monitoring as an objective technique for quantitating the frequency of silent ischemic episodes during daily life. Their article-notes that transient ischemia is more frequent and prolonged than is suggested by an analysis of chest discomfort alone. Positron emission tomography confirms that these episodes represent ischemia. Furthermore, the
M
majority of these episodes are unaccompanied by an increased heart rate, suggesting that an increased myocardial demand for oxygen does not play an important pathophysiologic role. Maseri et al discuss potential reasons why ischemia is silent in some patients and produces symptoms in others. The severity and duration of ischemia, neurophysiologic and psychologic differences between patients, and differences in pain thresholds all appear to be implicated. Miller describes the spectrum of silent ischemia in a variety of coronary artery disease syndromes, emphazing the role of vasoconstriction. Resnekov explores the potential roles of vasoconstriction, intramyocardial coronary arteries, and platelet aggregation. Various trigger mechanisms for silent ischemia are discussed, along with their clinical implications. Selwyn et al examine several clinical problems associated with silent ischemia. They raise important questions regarding the pathophysiology and prognostic implications of the frequent and sometimes prolonged episodes of silent ischemia in patients with coronary artery disease. Although numerous data are presented in this issue, it should be clear to readers that many questions remain unanswered. Should silent ischemia be actively looked for in groups of selected asymptomatic patients? Which patients are at high risk? Should high-risk patients be treated, and if so, how? In patients with angina and silent ischemia, it is tempting to try to minimize both phenomena. Certainly ischemia is an important adverse factor in all coronary syndromes in which it has been studied. Since silent ischemia occurs because of both an increased myocardial oxygen demand and a decreased supply, it may be important to select therapy that will affect both factors. Treatment with either calcium channel blockers, such as nifedipine, or nitrates, combined with beta blockers, may provide optimal anti-ischemic therapy. These and other questions will undoubtedly continue to challenge physicians for many years to come. It appears that careful therapeutic trials will ultimately be required to help clinicians decide how to best manage patients with silent ischemia.
From the University of California, San Francisco, School of Medicine, and the MoffittiLong Hospitals, Francisco, California. Requests for reprints should be addressed to Dr. William W. Parmley, Room Moffitt Hospital, University of California, 505 Parnassus Avenue, San Francisco, California 94143.
September
13, 1985
The American
Journal
of Medicine
Volume
San 1186,
79 (suppl
3A)