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A 59-year-old woman presented to Okinawa Chubu Hospital with a several-month history of progressive dyspnea. The patient initially noted exertional dyspnea after walking only a half-mile or when lifting heavy objects. Dyspnea worsened progressively, resulting in multiple syncopal episodes. The patient denied chest pain or dyspnea at rest. Her past history was significant for Ebstein anomaly, hypertension, hyperlipidemia, and duodenal ulcer. Her current medication included furosemide 20 mg twice a day, spironolactone 25 mg every day, losartan 25 mg every day, and pravastatin 10 mg every day. On initial examination, her blood pressure was 100/75 mm Hg, her heart rate was 75 bpm, and her respiratory rate was 18 breaths/min. A grade 4 systolic ejection murmur was noted throughout the precordium. Jugular venous pressure was not elevated and peripheral edema was not present. A chest roentgenogram showed cardiomegaly(Figure 1A)without pulmonary vascular congestion. An ECG showed normal sinus rhythm and marked left ventricular hypertrophy as manifested by high voltage and strain-type ST-T changes in I, aVL, V4 through V6(Figure 1B). Laboratory tests showed normal kidney and liver functions and no evidence of anemia, and brain natriuretic peptide was 399 pg/mL (

A 51-year-old black man without a personal or family history of cardiovascular disease was admitted to our hospital following syncope. Of note, he reported several episodes of chest pain and palpitations with lipothymia in the past few years associated with progressive dyspnea reaching New York Heart Association class II. ECG showed negative T waves in the precordium (V3 through V4) without significant ST deviation, monomorphic ventricular ectopies of septal origin with bursts of rapid polymorphic ventricular tachycardia, and mild first-degree atrioventricular (AV) block (Figure 1). Figure 1. A , ECG on admission showing negative T waves in the precordium (V3 to V4) without significant ST deviation, polymorphic narrow ventricular ectopies, and mild first-degree atrioventricular block. After β-blocker therapy was initiated, the patient was monitored showing a lengthening or PR interval. B , The patient received corticosteroid treatment with complete LV ejection fraction recovery at 3 months and partial conduction recovery with grade I AV block. AV indicates atrioventricular; and LV, left ventricular. Clinical examination and chest radiography were normal. Laboratory tests showed mildly elevated ultrasensitive troponin at 36 ng/mL, normal blood cell count, and C-reactive protein. Transthoracic echocardiography found interventricular septal hypertrophy (25 mm) without left ventricular (LV) dilatation or regional wall motion abnormality and no pericardial effusion, and the diagnosis of hypertrophic cardiomyopathy was suspected at the first step. β-Blocker therapy was initiated and the patient was monitored showing severe lengthening of the PR interval (Figure 1). Cardiac MRI found atypical and severe concentric right ventricular (RV) hypertrophy with diffuse elevation of myocardial signal on T2-weighted short tau inversion recovery images (Figure 2 Movies I and II in the online-only Data Supplement), and severe RV free wall hypokinesia along with global asynchrony of RV contraction. The LV ejection fraction was confirmed normal, whereas the RV ejection fraction was markedly impaired …

Background —Sudden death due to relatively innocent chest-wall impact has been described in young individuals (commotio cordis). In our previously reported swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mph baseball impacts to the precordium. Because activation of the K + ATP channel has been implicated in the pathogenesis of ST elevation and ventricular fibrillation in myocardial ischemia, we hypothesized that this channel could be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis. Methods and Results —In the initial experiment, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K + ATP channel, and chest impact was given on the QRS. The results of these strikes were compared with animals in which no glibenclamide was given. In the second phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fashion), with chest impact delivered just before the T-wave peak. With QRS impacts, the maximal ST elevation was significantly less in those animals given glibenclamide (0.16±0.10 mV) than in controls (0.35±0.20 mV; P =0.004). With T-wave impacts, the animals that received glibenclamide had significantly fewer occurrences of ventricular fibrillation (1 episode in 27 impacts; 4%) than controls (6 episodes in 18 impacts; 33%; P =0.01). Conclusions —In this experimental model of commotio cordis, blockade of the K + ATP channel reduced the incidence of ventricular fibrillation and the magnitude of ST-segment elevation. Therefore, selective K + ATP channel activation may be a pivotal mechanism in sudden death resulting from low-energy chest-wall trauma in young people during sporting activities.

Background Direct clinical manipulation to improve an impairment of left ventricular (LV) relaxation has not been reported. We investigated whether the LV relaxation rate in humans could be modulated by phase-controlled mechanical vibration applied to the patient's anterior chest wall and whether there are some quantitative differences in the responses of normal (N), hypertrophied (H), and failing (F) ventricle. Methods and Results In 46 patients (N, 10; H, 18 [hypertrophic cardiomyopathy]; F, 18 [heart failure]), the vibrator was attached to the precordium and a 50-Hz, 2-mm sinusoidal mechanical vibration was applied, with the timing restricted from the onset of isovolumic relaxation to end-diastole during cardiac catheterization. Heart rate and peak LV pressure showed no difference with vibration. However, in all patients, precordial vibration caused an acceleration of the LV pressure fall. The magnitude of the induced reduction of the time constant of LV pressure decay (ΔT) was larger ( P Conclusions Phase-controlled, small-amplitude vibration on the chest wall can directly modulate LV relaxation rate, especially in those with hypertrophy or failing ventricle.

A 66-year-old woman with no known medical history presented to the emergency department complaining of chest discomfort and difficulty breathing for the last 24 hours. She was in respiratory distress with a heart rate of 105 bpm and blood pressure of 115/65 mm Hg. The jugular venous pressure was elevated and there was a 4/6 holosystolic murmur across the precordium with a thrill. The ECG (Figure 1) showed acute anterior and inferior ST-segment elevation myocardial infarction (MI). The first total CK-MB fraction and troponin-I levels were 2001 U/L, 25.43 U/L, and 35 ng/mL, respectively. Coronary angiography …

A 7-kilogram 3-month-old boy was hospitalized with a 5-day history of high fever (>103°F), macular rash, strawberry tongue, and persistent irritability. A diagnosis of Kawasaki disease was made and the patient received 2 doses of intravenous immunoglobulin, prednisone, and high-dose aspirin. His platelet count was significantly elevated to 1.4 million/μL. Clinical examination revealed mild swelling of his fingertips and a diffuse macular rash. There was cervical and inguinal lymphadenopathy. The precordium was quiet and the first and second heart sounds were normal with no cardiac murmurs. The lungs were clear to auscultation and the abdominal examination was normal. A chest …

A previously healthy 37-year-old man had a sudden syncopal episode that lasted an estimated 10 seconds. The patient’s wife, who witnessed the event, said that his eyes rolled back and that he urinated but had no tonic-clonic activity. On regaining consciousness, he complained of dizziness, shortness of breath, and sweating. An emergency medical service then brought him to the hospital. In the emergency department, the patient complained of shortness of breath but denied chest pain, cough, fever, headache, weakness, or previous neurological difficulty. He had no significant past medical history and had been well before losing consciousness. On physical examination, the patient was alert and oriented but anxious and dyspneic. His oral temperature was 99°F; pulse, 115 bpm and regular; blood pressure, 105/70 mm Hg; and respirations, 20 breaths per minute. Cranial nerve function and optic fundi were normal. Neck veins were not distended, and the precordium was quiet, with normal heart sounds and no murmurs. Lungs were clear to auscultation. Abdominal findings were unremarkable, and the extremities had full, equal pulses with no edema. The chest radiograph and ECG obtained at entry appear in Figs 1⇓ and 2⇓, respectively. Arterial blood gas analysis (room air) disclosed a pH of 7.46, a Paco2 of 30 mm Hg, a Pao2 of 52 mm Hg, and an O2 saturation of 89%. Results of the following laboratory studies were normal: complete blood count; urinalysis; serum creatinine, calcium, phosphorus, and electrolytes; blood sugar and urea nitrogen; and liver function tests. Figure 1. Chest radiograph showing prominent central pulmonary arteries with abrupt tapering of the lower lobe branches (especially the left), possible …

A54-year-old white woman was referred for cardiac consultation because of increased dyspnea with exertion and leg pain. The patient’s past medical history was significant for smoking and recent onset of hypertension. On physical examination, she was found to have a blood pressure of 180/90 mm Hg and a heart rate of 110 bpm. The lungs were clear to auscultation. The carotid upstrokes were bounding, and there were bilateral carotid bruits. The central venous pressure was not elevated. The cardiac examination was significant for a loud, harsh systolic murmur (II to III/VI) across the precordium with radiation to the back. There was a left ventricular lift and a third heart sound. The abdominal examination was normal, and stool guaiac was negative. There was no peripheral …

A 29-year-old man with history of atrial tachyarrhythmias and a remote Potts anastomosis for treatment of tricuspid atresia presented with palpitations and chest pain. His medications included digoxin, furosemide, prednisone, methimazole, and amiodarone. He was afebrile. His pulse was 176 beats per minute with a blood pressure of 160/80 mm Hg. He was cyanotic with clubbed fingers and toes. The apical impulse was displaced to the 6th intercostal space in the mid-axillary line. Auscultation revealed normal S1, single S2, and a short systolic murmur arising from the Potts shunt that was heard over the left precordium and back. No diastolic component was appreciated. Chest radiography revealed cardiomegaly …

A23-year-old Haitian man presented with complaints of shortness of breath, dyspnea on exertion, and occasional palpitations. Examination revealed a wide pulse pressure and a continuous murmur across the precordium. The echocardiogram showed a ruptured aneurysm of the right sinus of Valsalva (Figure 1⇓). The sinus rupture dissected into the interventricular septum and then ruptured into the left ventricular cavity (Figures 2⇓ and 3⇓). No operative intervention was undertaken. Aneurysms of …

A 9-month-old previously healthy girl presented to the emergency room in congestive heart failure. The parents had previously noticed sweating during feedings with occasional increased respiratory rate. Physical examination showed her to be at less than the 5th percentile in weight and height for age, acyanotic, and tachypneic. Her precordium was hyperdynamic, with a normal S1, a narrowly split S2, a grade III/VI continuous murmur at the upper left sternal border radiating to the axilla and back, and a grade III/IV diastolic rumble at the apex. The liver edge was 3 cm below the costal margin. Pulses were normal and symmetrical. The ECG showed sinus rhythm, a right ventricular conduction defect, and left ventricular hypertrophy with ST changes …

Isopotential body surface distribution derived from 14 subjects with acute anterior and 14 patients with acute inferior myocardial infarction were studied to examine three possible difficulties with ST-segment summation methods as used for evaluation of infarction severity. First, recorded sums of potentials recorded from 150 electrodes placed on anterior and posterior thoracic surfaces and from five subsets of 42 electrodes located only on the left anterior precordium were compared. Lead subsets detected only one-half of total thoracic positivity in acute anterior infarction and the sums of potentials in these sets were significantly altered by small (approximately 1-1.5-inch) deviations in grid location. Second, differing isopotential distributions could yield nearly identical sums of potentials in left precordial electrode grids. Third, the effects of the wide variations in the normal ST-segment isopotential distribution were evaluated by studying 45 normal subjects and application of difference map and departure map and departure map techniques. The results illustrate the significant variation in potentials considered to be generated by the ischemic lesion caused by differences in control patterns. Thus, the recording of potential sums over limited torso areas, the attention to potential magnitudes rather than to distributions and the assumption that the normal ST segment is isoelectric represent significant problems in applying ECG methods to the quantitative evaluation of myocardial infarction.

To define the clinical significance of T wave map changes in patients with angina at rest, body surface isopotential T distributions were obtained in 48 patients with single-vessel disease (left anterior descending artery, 34; right coronary artery, eight; left circumflex artery, six) documented angiographically and were compared with those in 120 healthy subjects and those in 19 patients with left ventricular overload whose electrocardiograms showed negative T waves accompanied by an increase in R wave amplitude in left precordial leads. The T wave map abnormalities were observed in 24 of 48 patients (50%) with angina and were classified into three types: (1) type I (18 patients, 37.5%) was characterized by a segmental negative potential in the positive area located at the left thorax and the minimum at the peak of T wave positioned in the upper portion of the left anterior chest, (2) type II (three patients, 6.3%) was characterized by a negative potential with a minimum in the inferior thorax and an indentation of negative potential at the lower margin of the positive potential located over the upper thorax, and (3) type III (three patients, 6.3%) was characterized by a negative potential with a minimum at the back throughout the period of T wave. All patients showing T wave map abnormalities of type I had a significant stenosis of the left anterior descending artery. Likewise, all patients with type II or III had single-vessel disease of the right coronary or left circumflex artery, respectively. All types of T wave map changes observed in patients with angina were different from those in patients with left ventricular overload, whose maps showed the generalized negative potential at the inferior thorax and the left back and the minima clustered at the precordium. In seven patients with lesions of the left anterior descending artery, T wave map abnormalities of type I recovered to normal after successful percutaneous transluminal coronary angioplasty. The behavior of the negative potential and its extrema on the T wave map, which was not available from routine electrocardiography, was indicative of the involved coronary artery and probably of its associated ischemic area in one-half of our patients with angina pectoris.

Junctional depression is often observed during physical exercise in overtly normal subjects. To explore its pathogenesis, 15 normal volunteers were studied during supine, bicycle ergometer, submaximal stress tests. Electrocardiograms were simultaneously recorded from 42 electrodes on the left anterior precordium at two minute intervals at rest and during exercise. Data were used to construct isopotential maps throughout the P-QRS-T intervals. At rest, maps throughout the ST segment were dominated by a single maximum along the upper left sternal border. During exercise, all subjects developed junctional depression that was maximal along the lower left sternal border. Exercise maps during the early to mid-ST segment showed an intense minimum along the lower left sternal border that was continuous with terminal QRS forces in both intensity and location. Later in ST, this minimum decreased in strength and was replaced by a maximum located in the same area as that observed at rest. These observations suggest that junctional depression is the result of competition between two effects, one being normal repolarization which is obscured in the early ST segment by the second, possibly representing delayed terminal depolarization forces.

The theoretical background and limits of radiocardiography for the measurement of cardiac output, and of right ventricular and pulmonary blood volumes, are discussed. Injection of a known amount of radioiodinated (I131 ) human serum albumin (RIHSA) into the right atrium, and concomitant recording of a double-peaked time activity curve by means of a shielded scintillation detector placed over the precordium, allows measurement of cardiac output. The geometric arrangements that best approach ideal conditions are described. It is shown that the physiologic significance of the value for output as measured from the radiocardiograms varies with the indicator-flow ratio in 2 sides of the heart. The necessary conditions for measurement of right ventricular volumes from the radiocardiograms are presented, and the theoretical limits of the technic are evaluated. The problem of the measurement of pulmonary blood volume (PBV) from RIHSA radiocardiograms is-discussed. While it is not possible to make a direct measurement of mean PBV from RIHSA radiocardiograms, the limits within which the volume lies are indicated. (P.C.H.)

The electrocardiograms of patients with pathologic evidence of right ventricular hypertrophy and/or dilatation and exclusion of myocardial infarction are presented to bring out certain features likely to be mistaken for myocardial infarction: (1) abnormal qR or QS patterns or cove plane inversion of the T waves in leads from the right precordium; (2) reduction in the amplitude of the initial R wave or replacement by a QS deflection and/or change from an upright to an inverted T wave as the electrode is moved from the V 1 position to the transitional zone; (3) abnormal qrS deflections in leads from the left axilla.

A study of the precordial pulsations (kinetocardiograms) in patients with acute myocardial infarctions is presented. A paradoxic pulsation (bulge) over either the precordium or the epigastric area was noted in all patients studied.

The clinical, physiologic, and anatomic features of a special group of cases of total anomalous, pulmonary venous connection are reviewed. The occurrence of severe pulmonary venous obstruction in total anomalous pulmonary venous connection produces a characteristic syndrome: 1. Very early onset of dyspnea and heart failure. 2. Considerably more cyanosis than the usual case without obstruction. 3. Typical x-ray showing diffuse hazy lung fields with reticulated appearance without cardiac enlargement. 4. Electrocardiographic evidence of severe right ventricular hypertrophy with a tall R or qR pattern in lead V 1 and reversal of the R/S ratio over the precordium. 5. Physiologic findings of practically normal pulmonary flow, right ventricular and pulmonary arterial pressures greater than systemic, and a marked gradient between the pulmonary arterial "wedge" and right atrial pressures. 6. Rapid deterioration and death in the first weeks or months of life.

In an attempt to explain the electrocardiographic and other cardiac abnormalities in patients with muscular dystrophy, hemodynamic studies by right heart catheterization were done on 12 patients with muscular dystrophy. The study indicated the presence of latent congestive failure in some patients. An attempt to explain the abnormal QRS complexes and leads from the right side of the precordium in some of those patients is also made.

The instrumentation and procedure employed to secure radiocardiograms and the technic of analysis of the resulting curves are described. Time activity curves are recorded by means of a scintillation counter, with a NaI crystal 11/2 in. in dia. located in a lead collimator. Pulses from the photomultiplier tube are amplified and fed into a counting ratemeter and into a scaling circuit. The output of the ratemeter is fed into a multichannel electronic recorder, with monitoring oscilloscope. A solution of radioiodinated (I131) human serum albumin (RIHSA) or Kr85 is introduced into the right atrium by cardiac catheterization, and the resulting scintillation readings taken over the precordium are recorded along with the electrocardiogram. The curves are analyzed by reading at every 0.1 sec the height of the deflection in millimeters above the background. The latter is obtained by averaging over several seconds the ratemeter trace immediately before the curve. The net deflections are plotted on semilogarithmic paper against time on the linear abscissa. The downslope of the second peak is fitted with a single exponential. Various parameters needed for the calculations of right ventricular volume and pulmonary blood volume are discussed.

The electrocardiograms of patients in whom myocardial infarction was excluded at autopsy are presented to bring out the following features of left ventricular hypertrophy that may be mistaken for myocardial infarction: (1) QS patterns and/or abnormal RS-T elevation in leads from the right precordium; (2) abnormal Q waves, multiphasic QRS and/or cove plane inversion of the T waves in leads from the transitional zone; (3) prominent Q waves, marked RS-T depression and/or sharply inverted T waves in leads from the left axilla.

Body surface potential maps provide more detailed regional cardiac electrophysiologic information than the standard electrocardiogram. We performed a large-scale study of a normal population to form a comparison base for evaluation of the clinical utility of this technique. We analyzed body surface maps from 1113 normal subjects from 10 to 80 years old to detail map features as a function of age, sex, and body habitus. Maps were analyzed by visual inspection and by a spatial and temporal data reduction technique that allows statistical comparison of map features. On average, both QRS and ST-T potentials decreased with increasing age. Potential pattern distributions remained constant from 10 to 40 years. Beyond age 40, larger numbers of maps from normal subjects showed depolarization patterns consistent with delayed activation of the left anterior fasicle, despite normal 12-lead electrocardiograms. Only minor QRS potential amplitude and distribution differences were noted when male and female subjects were compared within groups of similar age and body habitus. Male subjects consistently showed greater average T potential amplitudes. Slender body habitus was associated with a more horizontal "zero" potential line. In female subjects over age 40 there were more extensive low-level negative potentials recorded over the precordium during the ST segment than in men. This study defines the range of normal body surface potential maps in a large clinically normal population and provides a basis for qualitative and statistical comparison with map features of patients with disease.

In order to assess the utility of contrast M-mode echocardiography in an intensive care nursery population of critically ill newborns with cardiac and pulmonary disease and to validate contrast echo methods, we performed 200 serial contrast echoes on 40 infants via umbilical arterial or venous catheters which had been placed into these infants for clinical indications. The resulting contrast echoes recorded from the precordium or the suprasternal notch allowed the delineation of intra- and extracardiac right-to-left and left-to-right shunting patterns. Patterns identified and validated by cardiac catheterization (in cardiac patients) were: right-to-left atrial shunts, right-to-left ventricular shunts, and left-to-right patent ductus arteriosus shunts. The studies were without complication. Serial application of these echocardiographic techniques was extremely important in assessing changing physiology in these neonates. Contrast echocardiography adds physiologic flow information to the anatomical information available from M-mode echoes and is quite important in the diagnosis and sometimes in the management of critically ill newborns.

We studied tactile perception in palpation of the precordium to determine the frequency response of the hand and to improve, if possible, the sensitivity of the hand as a transducer for precordial movement. The threshold of tactile sensation was determined for 10 subjects by manipulating the amplitude of movement of an impulse generator at each of a series of frequency settings in the subaudible range (1-40 Hz.) Relatively gross movements were necessary to achieve threshold in the lowest frequencies. A more than four-fold increase in sensitivity was obtained by restraining the fingers with the application of a light but unyielding disc to their dorsal surface. Clinical application of this device permitted the easy perception of a systolic thrust as well as a rapid filling wave in normal adult subjects over the right ventricle at the left sternal edge, an area generally considered to be motionless by conventional palpation.

Body surface isochrone mapping was performed in 36 normal subjects and in 85 patients with previous myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, activation time was measured as the time from the onset of QRS to the peak of the R wave. The lead points where R waves were not observed were designated the "no R wave area" (NR area). Isochrone maps of normal subjects had a consistent pattern, with isochrone lines extending from the right upper anterior chest to the left anterior chest and then to the back. NR area was small and was located only on the right upper chest or the upper back. On the isochrone maps of patients with myocardial infarction, abnormal findings were observed; NR area was found in 26 of 28 patients with anterior infarction on the upper to middle anterior chest, in 13 of 22 patients with inferior infarction on the lower chest, and in 24 of 25 patients with anterior and inferior infarction on the upper to lower anterior chest. Activation time was delayed near the NR area (peri-NR area delay) in 37 patients. In patients with apical infarction, an islandlike zone of delayed activation was typically found on the left precordium. These abnormal patterns are considered to indicate local abnormalities in the activation of infarcted myocardium; the NR area indicates dead unexcitable scar, and the peri-NR area delay and islandlike zone of delayed activation indicate partially infarcted myocardium of slow activation. Patients with NR area had greater degree of left ventricular asynergy and lower ejection fraction than those without.(ABSTRACT TRUNCATED AT 250 WORDS)

After a brief discussion of the lead field concept and an illustration of its application using a Teledeltos paper model, studies carried out on patients, employing multiple electrode or grid arrangements located over the precordium and the left posterior chest, to obtain the sagittal component of cardiac electromotive forces (e.m.f.'s), are described. On the basis of these observations, a minimum of 15 properly arranged and connected electrodes should be employed in the anterior electrode system but fewer will be needed posteriorly. A scheme, using 63 electrodes mounted in sponge rubber, has been devised to simplify the grid arrangement.

A correlation of the clinical and electrocardiographic findings was undertaken in 110 cases which had in common the presence of deeply inverted T waves in central terminal leads centered about position 3 on the precordium. The results of this study are reviewed. A summary is presented of changes encountered at the time of necropsy in nine cases in which electrocardiographic changes of similar type had been recorded. These observations are integrated with concepts derived from the dipole theory. The total evidence is viewed in relation to observations reported by other investigators.

It has been suggested that a tentative preoperative decision favoring a pericardial lesion, on the one hand, or a myocardial lesion, on the other, may be made from certain noninvasive procedures, including the electrocardiogram. An attempt was therefore made to detect associated myocardial fibrosis by electrocardiogram in 67 patients with constrictive pericarditis as proven at catheterization (63 patients), surgery (64 patients) or postmortem examination (12 patients). Seven of the 67 had electrocardiograms characteristic of, and 16 compatible with, old myocardial infarct. The electrocardiographic experience was otherwise typical of the literature with non-specific changes in the T waves or RS-T segments and/or low voltage in the remaining 44. All three autopsied patients whose electrocardiograms were interpreted as diagnostic of an old myocardial infarct and both autopsied patients with electrocardiograms compatible with that diagnosis showed myocardial fibrosis. In seven autopsied cases with non-specific T waves or low voltage, the myocardium was normal in three while four showed myocardial fibrosis. It appears that in a few cases right ventricular hypertrophy might have simulated infarct by inducing tall R waves over the right precordium, or R waves which decreased in amplitude as the electrode was passed from the right to the left precordium. Pathologic evidence related myocardial fibrosis to: (1) direct subepicardial penetration by the inflammatory process or deposit of fat in the subepicardial myocardium; (2) compromise of coronary blood flow, as by (a) direct throttling of coronary arteries by scar tissue or (b) deficient irrigation of subendocardial layers due to rigidity of the pericardium; or (3) a concomitant myocardial and pericardial process (lupus, radiation fibrosis, rheumatoid). Independent pericarditis and coronary disease was surprisingly rare. This limited experience (1) suggests that, though myocardial fibrosis may be predicted in constrictive pericarditis if the electrocardiogram shows characteristic changes of myocardial infarction, non-specific T wave changes or low voltage may likewise be associated with myocardial fibrosis, and (2) emphasizes that the difficulty in determining the site of a constrictive process may be compounded by the co-existence in the same heart of both a pericardial and a myocardial process.

The electrocardiograms before and after operation have been compared in 20 patients undergoing left mastectomy and in 19 patients undergoing right mastectomy. There are highly significant increases in the amplitude of the QRS complexes recorded over the precordium after left mastectomy, except in lead V 6 . There are highly significant increases in the amplitude of the QRS complexes of leads V 3R and V 1 after both left and right mastectomy. These data are not completely explained by a diminution of distance between the recording electrode and the myocardium or of electrical resistance following the excision of soft tissue. The possible relationship is suggested between the precordial voltage changes and the altered thoracic volume conductor.

After a peripheral injection of Technetium-99 m , an Anger scintillation camera placed over the precordium of nine patients without and three patients with hemodynamic abnormalities was used to record in rapid sequence the flow of the injected material through the central circulatory system. After the data were processed as sequential frames of digitized spatial matrices, the position of various chambers or compartments was identified and dilution curves from six sites were obtained, providing a series of input-output relations through the central circulatory system, i.e., superior vena cava, right atrium, right ventricle, lung, left atrium, and left ventricle. These relations were assumed to be cascaded as a series of first order lag systems, with or without time delay, on an analog computer, which allowed estimation of the time constant of the transfer function of each chamber or compartment (volume/flow) by reducing the problem to a consecutive, one-parametric manipulation. Measurement of the flow rate through the series (cardiac output) permitted the volume of each chamber to be estimated. Results correlated well with mean values established by other methods.

The recent development of the instantaneously sensing Anger scintillation camera, capable of recording wide-field radioisotope images from the precordium, and a system for video storage and analysis has provided a means of visualizing the anatomic and hemodynamic features of the heart and great vessels without the hazards involved in introducing a radiopaque agent. Sodium pertechnetate ( 99m TcO 4 - ) produces no cardiocirculatory effects or untoward actions and delivers only 0.13 rads of total body radiation. Following injection, the rapidly changing distribution of radioactivity within the heart is recorded by the scintillation camera-television system which includes no inherent dead time or overlap of the scanned field from frame to frame. Video tape replay is available immediately and sequential integrated pictures are possible at any rate up to 60 sec. Radioisotope images of longer intervals are easily obtained by the integration of successive stop-action fields reproduced on a high resolution television monitor and photographed on rapidly developed film. In addition, the replay may be gated and tracked, allowing selected phases to be integrated and time-concentration curves of blood flow. Five to 10 millicuries of 99m TcO 4 - in 2 to 8 cc were rapidly injected into selected cardiac chambers at the time of diagnostic catheterization in 50 patients with a variety of congenital and acquired forms of heart disease. Movement of radioisotope closely reflected the hemodynamic alterations caused by these conditions, as determined by standard contrast angiocardiography. The radioisotope-angiocardiogram provides a new approach for visualization of the cardiovascular system, does not require the use of radiopaque medium, is safer than angiography, and does not disturb circulatory function.

A case of myxoma of the right atrium with physiologic, surgical, and angiocardiographic findings has been presented together with a review of 6 other published cases. Several findings have been emphasized that may call attention to the possible diagnosis of right atrial myxoma: right-sided heart failure; intracardiac calcification of the right heart; enlargement of the right ventricle and right atrium; electrocardiographic findings of a prominent P wave and low voltage over right precordium simulating that found in Ebstein's anomaly and marked variation in heart rate not related to any physiologic event or change in rhythm; use of intracavitary electrode catheter to rule out Ebstein's anomaly; and finally, analysis of the right atrial curve may lead one to suspect that other than valvular stenosis is present. Angiocardiography gives a definitive diagnosis. Cure may now be obtained with surgical removal of myxomas; therefore, it is important that they be detected during life.

A new technic is described for the detection of left-to-right shunts. A miniature Geiger-Müller tube is placed in the esophagus behind the left atrium and positioned by the electrocardiogram. In this position the G-M tube measures radioactivity from the left atrium. Curves are then recorded simultaneously from the precordium, lung, and left atrium. Methods of injection, monitoring, and recording are presented that provide greater diagnostic accuracy over those external detector technics currently in use. Of 23 patients studied, 11 presented left-to-right shunts. Eight of these 11 patients were submitted to surgery; all were studied preoperatively and seven were studied postoperatively. Seven of the 11 shunts were detected by both precordial and esophageal technics. Four of the 11 shunts were missed by conventional precordial technics but were correctly diagnosed preoperatively by the esophageal detector. In addition, one shunt, which remained open postoperatively, was demonstrated clearly by the esophageal technic but was not indicated by the precordial curves. In no instance was the precordial curve positive for left-to-right shunt when the esophageal curve was negative. Although the accuracy of any radioisotope detection technic with external counting may not approach that of direct cardiac catheterization, this method, because of its relative simplicity and accuracy, is useful in the demonstration of left-to-right shunts both preoperatively and postoperatively.

T-wave inversion, in leads localized to a small segment of the precordium, has in rare instances been described as a normal variant. The present report concerns a number of individuals in whom more or less similar T-wave changes developed under circumstances suggesting myocardial ischemia, and who went on to develop acute infarction of the anterior wall of the heart. This may be a clinical analogue of the brief T-wave inversion which has been observed early in experimental coronary artery compression.

Within a few minutes after its onset, intense pain of acute myocardial infarction was abolished by briefly spraying the precordium with ethyl chloride. Prompt relief of pain did not prevent tissue necrosis, but may have ameliorated the clinical course. We infer that the stimulus for pain in acute infarction is of extremely short duration but gives rise to a secondary, self-sustaining pain cycle which may be terminated by altering the flow of nerve impulses from the skin. The case also illustrates the increased susceptibility to digitalis which develops some days after myocardial infarction.

A new electrode arrangement for the administration of elective direct-current countershock was studied, in which one electrode was placed in the esophagus, adjacent to the heart, and the other on the precordium. Thirteen patients with chronic atrial fibrillation were converted to sinus rhythm by the esophageal technic. Though the majority were, on clinical grounds, difficult cases for conversion, 11 were converted with shocks of 40 watt-seconds or less, and two with 60, after 40 failed. Five patients were defibrillated by both the esophageal and the conventional, anteroposterior chest technics; the energy requirement with the esophageal method averaged less than one third of that with the conventional one. Four patients received 40, and one 30 watt-second shocks without anesthesia; all five tolerated the shocks well, and three of four who had had countershock previously under anesthesia, expressed preference for the esophageal technic without anesthesia in the future. All patients were observed carefully for any symptoms suggestive of esophageal injury or dysfunction. None such occurred, either immediately or within 4 months. We conclude that this technic may have a place in elective countershock in that it may allow cardioversion to be undertaken in many patients who would otherwise require anesthesia.

The effect of pressure against the chest wall in the use of the stethoscope for both the bell and the diaphragm chest piece is discussed. A modified diaphragm chest piece in a single head designed to increase the auscultatory discrimination is discussed. Comparison of the modified and conventional diaphragm chest pieces on an artificial precordium and with the employment of accepted engineering principles in the study of sound revealed the superiority of the modified diaphragm.

A method for taking tracings which represent actual movements of the precordium (displacement curves) or records which show waves proportional to the velocity of movement of the chest wall (velocity curves) is described. The equipment employed is readily available, and the method is easy to use. The displacement curves are nearly identical with cardiograms taken with a good optical setup, and they may have diagnostic value. The velocity curves are more closely related to the functional status of the myocardium. The clinical significance of these tracings, especially the former, is pointed out.

Precordial movements starting after P and before Q have been studied. Right atrial contraction appears to cause a forward-rightward motion and left atrial contraction a backward movement of the precordium. The latter is exaggerated in most patients with mitral stenosis and in some patients with myocardial failure.

A versatile four-electrode single-channel system is described which is useful for precise research measurements of mirror patterns on the intact human subject, and the theoretic significance of results obtained on normal subjects for the QRS complex is presented in detail. It is concluded that the QRS complex at all points on the body of normal human subjects, including the precordium, can be considered to arise from a fixed-location equivalent heart dipole to an average accuracy of 5 per cent. Therefore, the "proximity" potential concept is untenable for the normal QRS complex.

PRIMARY intracardiac tumors of theheart are rare. The commonest primarytumor is myxoma, found almost exclusivelyin the atria, 75 or mnore occurring in theleft atrium. Mahaim' reported 200 primarycardiac tumors in 1945, from the world liter-ature up to that time. Strauss and Merliss2reviewed 480,331 autopsies from the LosAngeles County Hospital and were able toreport 8 cases of myxoma occurring in theleft atrium.Myxoma originating in the ventricles ap-pears to be extremely rare. A well-doeu-mented pathologic study of a left ventric-ular myxoma with embolic occlusion of theabdominal aorta and renal arteries was pub-lished by Young and Hunter3 in 1957. Thepatient was a 10-year-old girl diagnosed ashaving rheumatic heart disease because ofher cardiac disability and a rough mitralsystolic murmur transmitted to the axillaand over the precordium. At autopsy