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An attempt has been made to determine the wasted cardiac work involved in paradoxical outward motions of the precordium. The upward displacement during systole of a known weight placed on the apical area has been measured in (a) persons with normal hearts, (b) patients with ischemic heart disease, and (c) patients with disorders that place an increased load on the left ventricle. Reasons for the opinion that the values obtained for wasted left ventricular work are falsely low have been cited. The procedure did not cause consistent changes in useful cardiac work, which was serially measured in a few subjects with and without the weights on the chest. In the normal control subjects, the levels for wasted work varied between 0.1 and 5.3 gram-meters per beat, and the median was about 2.5 per cent of the normal useful (pressure × flow) work of the left ventricle. The data for patients who, in the absence of a precordial weight, had normal tracings of chest-wall motion (kinetocardiograms) were usually within the normal range or only slightly above it. The patients who, without added weight, displayed paradoxical motion had values for wasted work of 5 to 45 gram-meters. Calculations were also made of the wasted stroke effort, i.e., the integral of the wasted work. The range and median for the subjects with normal hearts were .07 to .37 and .23 gram-meter seconds, respectively. Again, some of the patients were within the normal range, but those with pronounced systolic outward motion had values that were markedly elevated, and up to more than 30 times the normal median. Cardiac catheterization was performed in 9 of the 13 patients who had lesions that caused left ventricular overloading. In 6 of these subjects the wasted stroke work exceeded 9 per cent of the useful work (mean aortic pressure × measured stroke volume), and in 3 the wasted work was more than 24 per cent of the useful work of the same subject. The highest value found was 44 per cent of the normal value of 100 gram-meters per beat and 31 per cent of the patient's left ventricular useful stroke work. Calculations from the data suggest that in some patients with severe heart failure the work wasted in paradoxical systolic movements may equal the useful work. In patients at rest the cardiac inefficiency, as judged by wasted work, appeared to parallel the clinical state more closely than did the cardiac performance, as judged by useful work. It is concluded that in some patients the work wasted in causing paradoxical systolic motion is sufficient to cause pronounced impairment of myocardial efficiency. The term ventricular dyssynergy is applied to this condition, in which a portion of the energy generated by some of the fibers is diverted to stretching others. Some possible implications of this concept are discussed. Chief among them is the realization that, although knowledge of the performance (pressure and flow) of a given heart is very helpful, additional information concerning efficiency is essential for complete evaluation of its functional state.

Recently the focus of the coronary care unit has shifted from resuscitation to prevention of cardiac arrest. From the data presented in this paper it appears that careful application of this policy will result in a one-third reduction in mortality among hospitalized patients with acute myocardial infarction. This result is achieved mainly by reducing the number of deaths due to unexpected catastrophic cardiac arrhythmias, e.g., primary electrical failure of the heart. Premonitory arrhythmias which herald the onset of such a catastrophe are defined as “arrhythmias of electrical instability” (multiple ventricular premature beats and ventricular tachycardia), and “arrhythmias of potential electrical instability” (bradycardia and heart block). Evidence is presented to show that aggressive treatment of these disorders should be employed. In this series of 300 hospitalized patients, death from myocardial infarction usually was due to overwhelming myocardial injury resulting in shock or pulmonary edema. Patients with this syndrome who do not respond immediately to catecholamines, digitalis and other routine measures carry an extremely poor prognosis; presently available methods have not significantly altered mortality in this group. Definitive treatment of intractable pump failure awaits the development of new technics such as circulatory assist devices. Immediate further reduction in mortality from acute myocardial infarction requires intelligent application of what has thus far been learned in the coronary care unit. Since sudden death prior to hospitalization, possibly due to arrhythmia, is still the chief cause of death from coronary occlusion, it follows that institution of coronary care unit technics closer in time to the onset of infarction may result in further salvage of life. The concept of “precoronary care” encompasses those measures required to effect this salvage. These include immediate hospitalization on mere suspicion of myocardial infarction, early electrocardiographic monitoring in emergency wards and in ambulances, and ultimately continuous telemetric monitoring of high-risk patients as they go about their daily tasks. Finally, it is clear that improved methods are needed for diagnosing myocardial infarction and for grading the severity of an attack. Standardized criteria should be established which will allow the vast accummulation of information currently pouring forth from coronary care units to be utilized in improving treatment of the disease.

Fifteen patients with a procainamide-induced lupus-like syndrome have been studied. On the basis of clinical manifestations, three groups were recognized: (1) An asymptomatic group of 4 patients; (2) a group of 5 patients with abnormalities limited to joints; and (3) a group of 6 patients demonstrating the more classic syndrome of systemic lupus. All patients had elevated serum titers of antinuclear antibodies, and 11 had positive LE cell preparations. The syndrome developed as quickly as two weeks after institution of procainamide and with as small a dosage as 0.75 gm. daily. After the drug was discontinued, clinical and serologic findings receded rapidly. It required from several days to five weeks for symptoms to disappear. In 2 patients, however, the manifestations were long-lasting even after discontinuation of procainamide. The immunologic reaction to procainamide occurs frequently. It is suggested that all patients receiving this drug have periodic blood determinations for circulating antinuclear factors.

In the past two decades there have been momentous advances in the care of patients with cardiovascular ailments. Yet, mortality from coronary-artery disease has remained unaffected. Year after year myocardial infarction and its complications exact the highest toll of any single disease. 1 In large metropolitan hospitals, the death rate from this condition 30 years ago ranged from 30% to 40% and remains unaltered today. Certain facts are forcing reevaluation of the problem. Peak mortality occurs at the very onset of myocardial infarction and then recedes almost exponentially, with 65% of deaths occurring in the initial three days and 85% during the first week of attack. Arrhythmias probably account for 40% of deaths. Of these about two thirds are due to ventricular fibrillation and one third to bradycardia, heart block, and asystole. 2 It is well established that these electrical catastrophes are usually not due to irreversible cardiac damage. On