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During a 4-year period, 33 patients with angiographic coronary artery spasm in the absence of significant fixed occlusive disease were reviewed. Sixteen patients had typical variant angina and 17 had catheter-induced spasm. All patients had one or more episodes of rest angina. Left ventriculography demonstrated mitral valve prolapse in 14 patients (42%) and end-systolic cavity obliteration in six (18%). Spasm was demonstrated to occur in the right coronary artery in 26 patients and in the left coronary artery in seven. Two patients had multivessel spasm. Comparing patients with variant angina and catheter-induced spasm demonstrated no significant difference in clinical, ECG, or angiographic parameters. Two patients with catheter-induced spasm had healed myocardial infarctions and both developed spontaneous non catheter-induced spasm in the infarct vessel. The majority of patients responded to long-acting nitrate therapy, though those with catheter-induced spasm tended to have more recurrent chest pain. Six patients were placed on calcium antagonist drugs with marked symptomatic improvement in five. This study suggests that patients with catheter-induced spasm are similar to those with variant angina and its angiographic documentation may be a marker for the identification of patients with vasospastic angina.

The purpose of this paper was to describe some instances in which there may be loss of electromotive force (emf) from myocardial tissue without biologic death of the tissue. Myocardial tissue which is electrically inactive although viable is considered to be electrically silent. Electrically silent myocardial tissue may, under the proper circumstances, regain electrical activity. The development of areas of electrical silence within the myocardium may be associated with electrocardiographic alterations, particularly pathologic Q waves. Such Q waves disappear after the area of electrical silence recovers. It is important to recognize the fact that loss of cardiac emf is not synonymous with tissue death. Judgment concerning the extent of a myocardial infarction or the significance of pathologic Q waves (or other changes in the QRS complex) in patients with tachycardia, angina pectoris, or electrolyte disturbances should take into consideration the possibility of the presence of electrically silent areas. Furthermore, awareness of the electrocardiographic alterations associated with electrically silent areas of myocardium provides an understanding of some difficult electrocardiographic problems and makes it unnecessary to invoke alterations in rotation, position, or sequence of depolarization to explain electrocardiographic findings which do not correlate with the autopsy data.

An electrocardiographic syndrome has been described which allows fairly reliable prediction of the presence of infarction of the left ventricular anterolateral papillary muscle. The changes in the electrocardiogram generally fall into three major groups. One consists of moderate to marked depression of junction J in the middle and left precordial leads associated with a concavity-upward deformity of the ST-T interval. Another consists of changes in the same leads with, however, slight depression of junction J and a convexity-upward deformity of the ST-T interval and terminal inversion of the T wave. The third consists of changes in these leads with, however, an extremely marked depression of junction J, associated usually with slight initial convexity-upward deformity of the ST-T interval. The presence of apparent T-U segment depression or U-wave inversion was detectable in the majority of electrocardiograms in all three groups.

Emphysema is frequently complicated by the presence of heart disease other than cor pulmonale. This association raises many problems in diagnosis and treatment. One is frequently confronted with a patient complaining of dyspnea who is noted to have a barrel chest, distended neck veins, palpable liver, hyperresonant percussion note, pulmonary râles, loud pulmonic second sound, and ankle edema. These findings might be due either to diffuse obstructive pulmonary emphysema or to left ventricular failure with simple, coincident, nonsymptomatic senile emphysema. The differentiation is obviously important. In this discussion, clinical guide lines are presented which are helpful in making this distinction. Pertinent points in the history include orthopnea, paroxysmal nocturnal dyspnea, exposure to respiratory irritants, and the duration and course of the symptomatology. Helpful physical findings include diaphragmatic excursion, retraction of rib margins, type and location of the cardiac impulse, gallop rhythms, pulsus alternans, characteristic râles, mechanismal disturbances, and type of neckvein distention. Laboratory data of importance are the electrocardiogram, chest x-ray film, circulation time, blood-gas determinations, and pulmonary function studies. When emphysema and heart disease coexist, problems in treatment are compounded. Problem areas noted in this discussion include the use of: sedatives, analgesics, and tranquilizers; bronchodilators; antibiotics and anticoagulants; oxygen therapy; phlebotomy; cough suppressants; diuretics; adrenal steroids; fluid and electrolyte therapy; compression belts; antihypertensive agents and digitalis.

The function of the papillary muscles to restrain the mitral valves is obvious. However, the dynamic nature of this function is not always appreciated. Failure of one or both papillary muscles to shorten during the ejection phase of ventricular systole, fibrosis, and atrophy of a papillary muscle or centrifugal migration of the papillary muscles due to left ventricular dilatation result in mitral incompetence. Depending upon the etiology of the papillary muscle dysfunction, apical systolic murmurs of varying characteristics may be heard. In general, a noncontracting papillary muscle in a normal-sized heart is associated with a murmur which is late in onset and crescendo-decrescendo in quality, whereas in the dilated heart the murmur is early, beginning with the first heart sound, and may be decrescendo, plateau, or crescendo-decrescendo in quality. Obviously, the murmurs of papillary muscle dysfunction may vary considerably depending upon the nature of the dysfunction and time course of activation of the muscle and other portions of the ventricular musculature. Associated electrocardiographic abnormalities may also occur. Mitral insufficiency due to acquired or congenital valvular disease has been exhaustively studied. On the other hand, mitral insufficiency secondary to disease of the papillary muscles has been almost completely neglected. Nevertheless, since our description of the papillary muscle syndrome in 1963, 1 more than 20 papers dealing directly or indirectly with this syndrome have appeared. In the present review we have extended the original description of the papillary muscle syndrome to include a number of diseases which either clinically or at necropsy have been implicated in the production of papillary muscle dysfunction in the hope that attention will be focused on those diseases, in addition to circulatory insufficiency, which may result in papillary muscle dysfunction.

The use of intracardiac carbon dioxide in negative-contrast roentgenography as a diagnostic procedure in pericardial disease has been outlined. Its rationale, safety, indications, contraindications, precautions, and interpretative clues have been discussed. It is a useful, safe, simple, and rapid procedure when properly employed.

Observations have been made on the small blood vessels of the dermis and subcutis of the human finger tip and abdomen. Two types of vessels have been described—vessels which closely resemble those of most other organs, and a second type of vessel never before reported. Vessels of the second type are found predominantly in the vicinity of sweat glands, and are lined by endothelial cells with the following characteristics: (1) small, dense, rod-shaped granules in the cytoplasm; (2) large bundles of very fine filaments in the cytoplasm; (3) groups of small vesicles in the cytoplasm, each group enclosed by a membrane; (4) thicker than typical endothelium, the cells in contracted vessels being pyramidal or columnar in shape. A possible functional signficance of this specialized endothelium has been suggested.