Acute Coronary Episode Research Articles

Management of the Patient with Severe Angina Pectoris

Severe angina pectoris may be reduced to tolerable levels by suppressing below the pain threshold those factors elevating systolic blood pressure and heart rate and prolonging systolic ejection period. Their product parallels myocardial oxygen consumption (MVO 2 ) as noted in several excellent reviews. The level of this product associated with angina, the "angina index," defines the individual threshold for onset of angina. Prevention of angina-inducing physical and psychic stress is desirable, but often impractical, and the use of nitroglycerin preceding or following stress may lead to years of acceptable life. Prolonged, spontaneous, or readily induced angina, especially with a change in pattern, may be due to an acute coronary occlusive episode, whether defined as a prodromal period or an actual myocardial infarct. This form of attack requires close observation and appropriate care. The psychic stress-prone patient may repeatedly present a benign duplicate of such pain production, producing a diagnostic challenge. Routine protection of the angina patient, especially against arrhythmias, is discussed. Different therapeutic modalities for control of intractable angina are presented, many with promise, but those currently giving the best results are: (1) elimination of precipitating conditions, i.e. (a) brady- and tachyarrhythmias, (b) hypertension, (c) hyperthyroidism, (d) mechanical obstruction of ventricular outflow, and (e) heart failure (2) beta-adrenergic blocking agents, i.e. propranolol, with or without nitrates or nitroglycerin; and (3) surgical revascularization preceded by selective coronary angiography. The aortocoronary saphenous vein bypass has been effective in prompt relief of angina in patients with viable myocardium and potentially good flow in the distal artery, with acceptably low operative mortality from skilled teams. Mechanical efficiency and thus congestive failure may improve, and there is hope for increased longevity. Contraindications are poorly defined, especially as related to its performance in recent infarction of varying magnitude. With only 3 years' experience in determining long-term benefits, it seems rational to repeatedly redefine indications for surgery, but currently not to operate on every patient with "significant" coronary disease.

Cardiac diagnosis and decision-making in a hospital emergency room.

AbstractThe emergency room records of 140 patients with cardiac complaints were reviewed. The average age was 60 years. Chest pain was the most common symptom and a majority of patients with this complaint expressed fear of an acute coronary episode. Of 41 cases admitted with the initial diagnosis of myocardial infarction, only 21 had that diagnosis at the end of two weeks. Of 91 patients sent home from the emergency room, 83 were alive and well at the end of six weeks. A single patient died of acute myocardial infarction ten days after leaving the emergency room. No patient was averse to admission, and in 10 instances patients came to the emergency room equipped with personal items indicating anticipation of admission. Such studies are feasible and may elucidate further the role of the emergency room in the early care of the “coronary suspect.”

The Role of Effort in Coronary Occlusion-Reply

To the Editor:— May I note that my paper concentrated on the exertion and type of employment of the patient. Everyone realizes that mental or emotional strain may impose a burden on the circulatory apparatus. Are we to conclude from Dr. Hyman's statement that this strain causes acute coronary occlusion? Not in my opinion, but it may precipitate angina pectoris or acute coronary insufficiency without occlusion. It has been an uphill struggle to demonstrate that acute coronary occlusion, unlike other types of acute coronary episodes, is not precipitated by effort. At one time, I was a voice in the wilderness; now, this is an opinion of a multitude. In my first compensation case appearances, 1928 to 1930, I testified that coronary occlusion was precipitated by effort; this was then the commonly accepted belief. It was only when I began studying the patients in the wards of the old New York

Pericarditis following mild or silent coronary episodes: An attempt at narrowing the field of idiopathic pericarditis

“Coronary” pericarditis represents a syndrome consisting of pericarditis, pleurisy, and pneumonitis, which develops secondary to arteriosclerotic heart disease. It can be readily diagnosed when it follows shortly after a well-defined myocardial infarction. However, when the acute coronary episode is mild or silent, and there is a lapse of many weeks between the coronary attack and the appearance of pericarditis, the causal relationship may be obscured and idiopathic pericarditis diagnosed. Five cases are reported to illustrate this point. The search for etiology in any given case of pericarditis should include among other causes “coronary” origin. Diagnostic considerations of this kind will result in the separation of cases hitherto assigned to idiopathic pericarditis and in the reduction of this undesirable group.

The Diagnosis and Treatment of Acute Coronary Heart Disease Without Objective Findings

There are patients with acute coronary heart disease who have no objective evidence of myocardial infarction by electrocardiogram or laboratory tests, in fact who have no objective evidence of any cardiac change whatsoever. In such patients, the clinician, purely on a history as he obtains it, is faced with the necessity of making a diagnosis which carries with it at least initially, potential consequences of grave significance. The complexity of such a serious diagnosis is compounded by the fact that the history is usually atypical. It is such atypical histories that frequently lead to a reassuring pat on the back with some vague remark about “muscle pain.” It is also such histories that occasionally end with sudden death. Given a patient, middle aged or beyond, with a vague chest discomfort that has no diagnostically helpful relationship, and in whom there are no objective evidences of heart disease, one is faced in the first instance with the necessity of excluding acute coronary heart disease. In the usual situation any other diagnostic possibility is such that it can await the fullest possible consideration of the cardiac status. If an electrocardiogram can be recorded during the course of the pain, transient ischemic changes will occasionally be diagnostically helpful. If such changes are not observed, it is my belief that any suspicion of an acute coronary episode should justify a tentative diagnosis of acute coronary heart disease. The index of suspicion should be especially high in any patient middle aged or above who spontaneously develops chest or upper abdominal distress of any sort that is not clearly or easily identifiable as due to some non-cardiac cause. In such a situation one can do little more than conclude that it is impossible to eliminate acute coronary heart disease as a diagnosis. Therefore, it is impossible to exclude the possibility of sudden death, or of the development of a major myocardial infarction. Since such serious complications cannot be discounted, management must be directed accordingly. Even a known history of peptic ulcer or x-ray evidence of gallstones should be ignored initially unless the clinical picture can be surely related to these conditions. There should be no diagnostic difficulty when a patient presents himself with a history that is fairly typical of the pain of acute coronary heart disease but without objective findings. This includes patients with the onset of classical angina of effort, or the acute worsening of pre-existing angina. The typical history should suffice for a tentative diagnosis of acute coronary heart disease. The patient with an atypical history, however, may present himself with little more than mild to moderate substernal discomfort that comes and goes spontaneously and is often associated with belching and indefinite upper abdominal distress, in other words “indigestion.” The discomfort may extend into the neck. If the

Typical and Atypical Electrocardiograms in Myocardial Infarction Caused by Acute Coronary Occlusion and Coronary Insufficiency

When an acute coronary episode occurs, if the initial electrocardiogram does not indicate a coronary occlusion, it may be difficult at first to determine the exact nature of the attack. The electrocardiogram may remain normal for a variable period or may indicate coronary insufficiency and myocardial ischemia. In the cases going on to coronary thrombosis and massive infarction, the electrocardiogram may show various rapidly changing patterns before the appearance of RS-T elevation and Q-waves. In coronary occlusion the electrocardiogram often shows involvement of more than one surface and variations of the typical patterns are frequent. The changes may be present in only a few of the 12 routine leads or only in special chest positions. In an acute coronary episode it is essential to keep the patient at rest until the extent of myocardial involvement has been determined. Not infrequently the electrocardiogram shows temporary improvement or actual return of RS-T and T to normal between the third and 10th days following myocardial infarction.

Remarks on the Graphic Diagnosis of Coronary Disease

I . Typical and Atypical Electrocardiograms in Myocardial Infarction Caused by Acute Coronaqj Occlusion and Coronary Insufficiency The electrocardiogram has been epic making in the diagnosis of coronary occlusion and is the main reason for the ever increasing frequency with which this disease is detected. The ordinary electrocardiographic diagnosis has become so well-recognized that i t is now well to talk, not only of the typical electrocardiogram, but of the atypical electrocardiogram in myocardial infarction. I t is time also to divide the study of myocardial infarction into two types, (1) the subendocardial type, secondary to coronary insufficiency, that is, without complete occlusion of a coronary artery, (2) the through-and-through type caused by coronary occlusion, that is, complete obstruction of a coronary artery. Coronary insufficiency is usually associated with coronary sclerosis but may be observed in a normal heart, for example, following hemorrhage. In coronary insufficiency the electrocardiogram shows RS-T depression, T-wave inversion, or RS-T depression and T-wave inversion combined, since the damage is localized in the subendocardial region. For the same reason, the outlobk is much better in coronary insufficiency. The electrocardiographic alterations are usually transient, lasting a day or two, or one or two weeks or months ; rarely they are permanent. The T-wave inversions are not usually as deep as those seen in coronary occlusion. There are no Q-waves or RS-T segment elevations because there is no through-and-through infarction. I t may take a few days for the electrocardiographic changes to develop; hence, if an acute coronary episode of any kind is suspected the electrocardiogram should be repeated several times. The type of electrocardiogram just described, that is, with RS-T depressions and T-wave inversions, but without deep Q-waves, is also seen in the premonitory phase of a coronary occlusion. Obviously there is a partial occlusion which causes coronary insufficiency. I believe that, once the artery is completely occluded, the clinical and electrocardiographic picture of coronary occlusion appears, that is, RS-T elevation is seen immediately. Within the first 12 to 24 hours the characteristic deep Q-wave is not seen but one can almost discern i t if he looks intently. After 12 to 24 hours i t is usually quite obvious. In anterior wall infarction the deep Q and RS-T elevations appear in leads I, aVL and in chest leads. In diaphragmatic or inferior wall infarction these alterations appear in leads 11, I11 and aVF. In true posterior infarction, tall R-waves appear on the right side of the chest, i. e., in V1 and 2. Q-waves may be seen in Va, s, 7 or Vs. Doctor Jaffe has been in the forefront in the description of atypical changes in coronary occlusion. For example, in serial electrocardiograms, temporary improvement may occur.

Complete functional recovery after coronary occlusion and insufficiency.

Three decades have elapsed since coronary occlusion became widely recognized as a clinical entity. It is now possible, therefore, to have a comprehensive view of the acute attack and to study its subsequent course among the many patients who have survived. At first, only the severe attacks were recognized as occlusions and their mortality rate was high. The prognosis for all patients with coronary occlusion, therefore, was considered to be poor. Later, the introduction of early and complete bed rest, a low-calorie diet, and the discreet use of drugs saved many lives. 1 It is now relatively simple to recognize mild and atypical acute coronary episodes, from which the patient usually recovers. The mortality rate in first attacks of the disease is, at present, only 10% or less. As a result, the early pessimism concerning an acute coronary occlusion has gradually diminished. The progress of patients who have survived an

The diagnostic value of the pattern T 1 lower than T 3 (T 1 < T 3) compared with the information yielded by multiple chest leads in myocardial infarction

Sixty-six cases which presented the clinical picture of coronary disease and the electrocardiographic pattern T 1 lower than T 3, were studied in an effort to ascertain the diagnostic value of the pattern T 1 lower than T 3 as compared with the information yielded by multiple chest leads. In most of the cases, from four to six chest leads were taken; in some instances, also, points of the chest at a higher level were explored. In forty cases, an anteroseptal site of infarction was indicated by changes in the chest leads; in fifteen cases, anterolateral infarction was diagnosed. The pattern T 1 lower than T 3 was also observed in a single case of posterior infarction in the earliest stage when T 3 was unduly high prior to inversion. In nine cases, the site of the lesion could not be determined because the chest leads failed to show significant changes. The pattern T 1 lower than T 3 is observed in both the earliest stage of myocardial infarction and as a late sign; it may persist for many years after the acute coronary episode. It is no more specific for myocardial infarction or coronary disease than is inversion of the T wave. Among other conditions, it may be associated with pulmonary emphysema and even with a normal heart that is in vertical position. When these latter conditions have been ruled out, the pattern T 1 lower than T 3 is equivalent to the T 1 type of myocardial infarction in the great majority of cases. Whenever the pattern is observed in cases presenting a history of sudden onset or aggravation of anginal pain, it should strongly suggest an ischemic myocardial lesion. In nine cases, the pattern T 1 lower than T 3 was the prominent electrocardiographic change throughout the course of observation, while changes in the chest leads were inconspicuous or absent. This fact indicates that the ratio of amplitude of T 1 and T 3 may be a more sensitive index of a myocardial lesion than are changes of the T waves in Lead I, considered by themselves, or slight changes of T in the chest leads. Minor lesions in the anterior wall which cause only lowering of T in the chest leads may escape recognition unless they are indicated by reversal of the normal ratio of amplitude of T in Leads I and III. Also, lesions in the anterior or lateral wall close to the base of the heart may not be demonstrable in the ordinary chest leads but are suggested by the pattern T 1 lower than T 3. The finding of this pattern may lead to further exploration of the chest and, thus, to discovery of the site of the lesion.