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The best method for detecting early left ventricular (LV) dysfunction in patients with chronic aortic regurgitation is uncertain. Variables used previously to identify LV dysfunction have included (1) angiographic measurements to identify an LV end-systolic volume index (LVESVI) ≥60 ml/m 2 , (2) echocardiographic measurements to identify LV end-systolic dimension (LVESD) ≥5.5 cm or LV fractional shortening ≤25%, and (3) depressed LV ejection fraction (EF) at rest and/or an LVEF or LVESVI that deteriorates with exercise as detected by myocardial scintigraphic measurements. The hypothesis was tested that radionuclide ventriculography with exercise allows earlier detection of important LV dysfunction in patients with aortic regurgitation than the other variables. In 15 consecutive asymptomatic or only minimally symptomatic patients (8 men and 7 women, mean age 44 years) with isolated 2 to 4+ aortic regurgitation (1) rest and exercise-gated radionuclide ventriculography, (2) M-mode echocardiography, and (3) LV angiography were performed. No other cause of LV dysfunction was apparent in 13 patients; 1 patient had moderate systemic arterial hypertension and 1 had 50% luminal diameter narrowing of the proximal left anterior descending coronary artery. Ten patients did not have an increase in LVEF >0.05 EF units at peak exercise (0.58 ± 0.11 to 0.50 ± 0.12, mean ± standard deviation [SD]) (Group 2), whereas 5 had a normal LVEF response to exercise (0.63 ± 0.08 to 0.69 ± 0.07) (Group 1). Eight of the 10 patients with abnormal LVEF responses to exercise had a decrease in LVEF >10% during exercise. The same 8 patients also had an increase in LVESVI with exercise, whereas the 5 patients with normal LVEF responses to exercise had normal or blunted LVESVI responses to exercise. Only 4 of the 10 patients with exercise-induced LV dysfunction had an angiographic LVESVI ≥60 ml/m 2 , and only 1 had an echocardiographically determined LVESD ≥5.5 cm. Serial follow-up rest and exercise scintigraphic and echocardiographic measurements were made in 8 of the patients a mean of 9.4 months after the initial measurements; 3 patients were in Group 1 and 5 in Group 2. The 5 patients in Group 2 again demonstated abnormal LV function during exercise stress, and 2 of the 3 patients in Group 1 then demonstrated an abnormal LV functional response during exercise. Therefore, it is concluded that (1) exercise radionuclide ventriculography identifies LV dysfunction earlier than traditionally used assessments, (2) LV dysfunction appears to persist in patients that demonstrate it and develop in others that did not have it originally, and (3) echocardiographic dilatation of the LVESD to 5.5 cm appears to be a late and relatively unusual occurrence.

The clinical, left ventricular and coronary angiographic data, and the technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigraphic results are presented in 31 patients with unstable angina pectoris. One-third of these patients had positive 99mTc-PYP myocardial scintigrams in a pattern suggesting limited and diffuse subendocardial necrosis. The positive 99mTc-PYP myocardial scintigrams occurred without diagnostic electrocardiographic and cardiac enzyme changes suggestive of myocardial infarction; positive scintigrams seemed to occur more commonly in patients with continuing pain after admission and in those without previous history of myocardial infarction. The positive 99mTc-PYP myocardial scintigrams did not correctly predict coronary anatomical patterns except that positive scintigrams occurred only in patients with coronary artery disease. Neither did the positive scintigrams necessarily occur in that group of patients with the poorest ventricular function though the 2 patients with the lowest ejection fractions both had positive 99mTc-PYP myocardial scintigrams. Finally, when positive 99mTc-PYP scintigrams are the only evidence suggestive of limited subendocardial infarction in patients with unstable angina pectoris, they do not appear to have any prognostic significance in terms of longevity or response to pharmacological or surgical therapy, though the follow-up period so far is short.

At cardiac catheterization, the effect of isoproterenol on coronary blood flow was compared in six patients with primary myocardial disease and six patients who appeared to have no cardiac disease. Coronary blood flow was measured by selective coronary artery injection of xenon-133 and external monitoring of disappearance curves with a dual probe, digital scintillation counter. In the presence of similar changes in cardiac output and heart rate-systolic pressure product, changes in coronary blood flow and coronary resistance in response to isoproterenol were significantly less ( P < 0.05) in the subjects with primary myocardial disease than in the normal subjects.

Four cases are reported in which medically refractory and ultimately fatal ventricular tachycardia developed relatively late during hospital convalescence from acute myocardial infarction. All 4 had tachycardia refractory to combinations of antiarrhythmic agents, and they required almost continuous ventricular defibrillation. Mechanical circulatory assistance (Avco intra-aortic balloon pumping) proved ineffective in controlling the recurrent arrhythmias. Emergency cardiac catheterization performed in 3 patients and postmortem examination in the fourth patient demonstrated the following: (1) complete occlusion of the left anterior descending coronary artery near its origin and diffuse circumflex obstruction; (2) extensive myocardial infarction involving two thirds of the anterior wall; and (3) ventricular ejection fractions of less than 25 per cent. Emergency surgery also proved ineffective in 2 patients. These findings suggest that recurrent ventricular tachycardia developing late in the course of recovery from an acute myocardial infarction is an ominous prognostic sign in patients such as these. Mechanical circulatory assistance in combination with various antiarrhythmic agents appears to be of little benefit in controlling this type of ventricular arrhythmia.

Fifty patients with the clinical syndrome of unstable angina pectoris were evaluated. Twenty-seven were randomized into medical or surgical treatment groups and subsequently followed up. The results of the study reveal that: (1) there is approximately a 16 percent incidence rate of significant left main coronary artery disease in patients with this entity at our institution; (2) 10 percent of patients do not have angiographically significant coronary artery disease; (3) pain relief is better in the surgically treated patients, but the 1 1 2 year survival rate is not significantly different between the groups; (4) 50 percent of the medically treated patients again had the syndrome of unstable angina pectoris in the initial few months of the follow-up period; (5) the operative and late postoperative mortality rate in patients presenting with unstable angina pectoris and left main coronary artery disease in this small group of patients was 43 percent; and (6) four of six patients with this syndrome whose condition was deemed inoperable and who were not randomized died within the subsequent few months.

The influence of hypertonic mannitol on regional myocardial blood flow and ventricular performance was studied during acute myocardial ischemia in awake, unsedated and in anesthesized dogs and after myocardial infarction in awake unsedated dogs. Regional myocardial blood flow was measured with radioactive microspheres. Generalized increases in regional myocardial blood flow occurred after mannitol in all of the different animal models studied. The increases in coronary blood flow after mannitol were just as impressive in the nonischemic regions as in the ischemic portion of the left ventricle in all of the different models that were examined in this study. Improvement in regional myocardial blood flow to the ischemic area of the left ventricle after mannitol was associated with a reduction in ST segment elevation during acute myocardial ischemia in anesthetized dogs. The increases in regional myocardial flow after mannitol were also associated with increases in contractility, but the increases in flow appeared to be more impressive than the changes in contractility. The data obtained demonstrate that mannitol increases regional coronary blood flow to both ischemic and nonischemic myocardium in both anesthetized and awake, unsedated, intact dogs with acute and chronic myocardial ischemia and that mannitol reduces ST segment elevation during acute myocardial ischemia in anesthetized dogs. Thus the results suggest that under these circumstances the increases in regional myocardial blood flow after mannitol are of physiological importance in reducing the extent of myocardial injury. Since coronary blood flow increased to nonischemic regions the increases in regional myocardial flow demonstrated in this study after mannitol cannot be entirely explained by the mechanism of reduction in ischemic cell swelling.

Of the 27 patients described, 23 were in cardiogenic shock, 2 had severe left ventricular failure, and 2 had medically refractory ventricular tachycardia. Utilizing intraaortic counterpulsation, adequate systemic blood pressure was initially restored in 19 patients. Nine of these were subsequently weaned from circulatory assistance, but only three were discharged from the hospital and are currently alive. The remaining 10 patients who derived initial benefit from circulatory assistance were balloon-dependent in that they could not be weaned from circulatory assistance. Eight of these patients subsequently underwent cardiac catheterization; four had inoperable disease. The remaining four patients underwent surgery for either resection of the area of infarction and/ or for myocardial revascularization; only one survived to subsequently leave the hospital. Ventricular volumes were abnormal and ejection fractions were below 30 per cent in all the patients in cardiogenic shock except one who underwent cardiac catheterization and ultimately died. Ejection fractions were greater than 30 per cent in the two patients with cardiogenic shock who were weaned from balloon support and survived to leave the hospital without surgery. Both of these patients had inferior myocardial infarction. The data obtained from this experience suggest that intraaortic counterpulsation is a very useful adjunct to currently existing medical measures to treat both cardiogenic shock and medically refractory left ventricular failure but that most patients have such extensive disease that they can neither be weaned from balloon support nor undergo successful infarctectomy or myocardial revascularization.

This well-illustrated article considers the role of plain film examination of the adult patient with valvular heart disease caused by rheumatic heart disease. As stressed in Dr. Elliott’s article in this symposium, the importance of interpreting anatomic information within the physiologic framework provided by assessing the pulmonary vasculature cannot be overemphasized.

The influence of hypertonic mannitol on regional myocardial blood flow and ventricular performance in awake, intact, unsedated dogs with myocardial infarction resulting from chronic occlusion of the proximal left anterior descending coronary artery was studied. tmannitol given to increase serum osmolality 20 mOsm increased regional myocardial blood flow to that portion of the left ventricle supplied by the occluded left anterior descending coronary artery by 22 +/- 2.8% (1.06 +/- 0.19 to 1.36 +/- 0.23 ml/min with g-1) without changing the inner:outer wall flow ratio. Mannitol also significantly increased regional myocardial blood flow to other areas of the left ventricle and the ventricular septum. Mean aortic pressure, maximal LV dP/dt, LV dP/dt/P, and cardiac output also increased significantly after mannitol. Thus hypertonic mannitol increases regional myocardial blood flow and ventricular performance in the awake, unsedated dog with prolonged occlusion of the proximal left anterior descending coronary artery. The increase in regional myocardial blood flow after mannitol under these circumstances probably is at least in part secondary to the increase in blood pressure and contractility. The increases in regional myocardial blood flow after mannitol in this study are less impressive than those that have been previously reported in the setting of either no myocardial ischaemia or acute myocardial ischaemia; this is probably due to the vasodilatation that chronic myocardial ischaemia itself produces in the canine heart.

A new model is proposed for the quantitative analysis of segmental left ventricular wall motion from contrast left ventriculograms and scintigraphic cardiac-gated blood-pool images. This model was tested in dogs using implanted lead beads in the myocardium and contrast left ventriculography. Measured values of bead position and displacement were in good agreement with the estimated values determined by the model. Segmental left ventricular wall motion was also measured in 21 patients in whom both cardiac-gated blood-pool scintigrams and contrast left ventriculograms were obtained within minutes of one another. Wall motion values obtained using the end diastolic and end systolic frames of the gated blood-pool studies and the contrast left ventriculograms correlated favorably in the 60 degrees left anterior oblique view.

1. Because of anatomic similarities between the splanchnic circulations of man and the rabbit, the rabbit was selected as the subject for experiments involving the nature of splanchnic blood flow after ligation of the superior mesenteric artery.2. Collateral flow to the obstructed superior mesenteric artery is established almost immediately, as demonstrated by contrast aortography, and circulation usually diminishes until the animal dies. Clotting of blood in mesenteric and collateral channels does not appear to play a role in mortality, for heparinization is not effective in prolonging life.3. A possible mechanism contributing to bowel ischemia in superior mesenteric artery obstruction is the opening of arteriovenous shunts. Supporting evidence includes opacification of the portal and mesenteric venous systems in experimental animals, which is not observed in control animals who have had repeated arteriography. Additional evidence is offered by portal venous blood oxygen saturation studies performed befo...

The observation of diminished motion of the anterolateral wall of the left ventricle in patients with mitral stenosis initiated this study. Twelve patients with mitral stenosis, 4 with right ventricular enlargement of other origin, and 8 normal subjects formed the basis for a quantitative analysis of the left ventricle by left cineventriculography. Our study indicated a markedly impaired contractility of the anterolateral wall of the left ventricle and posterobasal area in our patients with mitral stenosis. The 4 patients with right ventricular enlargement showed the same phenomenon of the anterolateral wall, but an abnormality of the posterobasal area was not evident. A reduced ejection was found in both groups. Our study further implicates a myocardial factor as a cause of reduced cardiac output in mitral stenosis. Lastly, as a potential explanation, we postulate that right ventricular enlargement, in some patients, may produce secondary abnormalities of left ventricular contractility.

The diffusible-indicator method of determining tissue blood flow was devised by Kety and his associates, 1–3 who observed the washout of an intraarterially injected tracer from the tissue of interest, and found that it was proportional to tissue blood flow. Kety's original tracer was nitrous oxide, but he soon adapted his method to the use of 24 Na. Other investigators developed Kety's method further, substituting 85 Kr, and ultimately, 133 Xe as diffusible indicators. It has been found that if 133 Xe is injected directly into a coronary artery and its washout from myocardium is observed with a scintillation probe over the precordium, the resulting determination, mean myocardial blood flow, is of limited application. Since coronary artery disease is a regional process, the most useful determination is one that yields regional myocardial blood flow. This may be determined by one of the original Kety methods, 3 i.e., observing the washout of tracer injected directly into the myocardium, but since it requires thoracotomy this method is not widely applicable. Several groups have assembled instrument systems based on the use of scintillation camera-computer combinations with which they can enter the image of the passage of a bolus of intracornoary arterially injected tracer, and by means of image data quantification derive regional myocardial blood flow values by Kety's method. The authors have studied more than 130 dogs before and after experimental coronary embolization and have described a complete method of deriving regional myocardial blood flows with an Anger camera-small computer system. Analysis of flow curves thus generated has suggested the existence of more than one compartment within myocardial blood flow. These compartments might be related to primary/collateral flow or to the volume of perfused tissue incorporated in the region of interest. Cannon et al. 25–27 have employed a multicrystal camera of the autofluoroscope type and an IBM 360/91 computer, in which the camera functions as 294 isolated detectors for the purpose of identifying as many regions of myocardial blood flow. Cannon et al. have studied both normal human subjects and patients with radiographically demonstrable coronary artery disease and have found regional flow to be a valid method both for identifying the myocardial flow inhomogeneities expected with coronary artery disease and for evaluating the results of reparative surgery.

This study correlated levels of activated fibrinolysis with the presence, extent, and rate of resolution of angiographically documented pulmonary emboli. Pulmonary emboli demonstrable by angiography were associated with detectable fibrin split products in the serum of 24 of 25 patients. In the absence of increased fibrin split products, pulmonary emboli large enough to be demonstrated by angiography were found in only 2 of 25 positive pulmonary angiograms. Spontaneous resolution of pulmonary emboli could not be correlated with the the concentration or persistence of fibrin split products but did correlate well with the presence of a reversible precipitating cause. Thrombophlebitis in the absence of clinical evidence of pulmonary embolism was not associated with increased concentrations of fibrin split products in eight of nine patients. The one patient with increased fibrin split product concentration had evidence on lung scan of silent pulmonary embolism.

At cardiac catheterization, the effect of isoproterenol on coronary blood flow was compared in six patients with normal coronary arteries and normal left ventricular function, and eight patients with angiographically defined coronary lesions. Coronary blood flow was measured by selective coronary artery injection of xenon-133 and external monitoring of disappearance curves with a dual probe, digital scintillation counter. Resting values did not differ in the two groups. In the normal group isoproterenol increased mean coronary blood flow 93 ml/100 g/min (152%) and cardiac output 2.3 liters/min (42%); coronary resistance/100 g decreased 60 ± 4% ( sem ), while total peripheral resistance decreased 29 ± 4%. In the coronary disease group coronary blood flow increased 20 ml/100 g/min (33%) and cardiac output increased 2.8 liters/min (62%); coronary resistance decreased 26 ± 9% and total peripheral resistance decreased 37 ± 4%. In all normal patients the percent increase in coronary blood flow markedly exceeded the percent increase in cardiac output and the percent fall in coronary resistance markedly exceeded the percent fall in total peripheral resistance. In six of the eight patients with coronary lesions the percent increase in coronary blood flow was less than the percent increase in cardiac output and the fall in coronary resistance was less than the fall in total peripheral resistance. Thus measurement of coronary blood flow, cardiac output, and aortic pressure before and during isoproterenol infusion may permit differentiation of those subjects with physiologically significant coronary obstructions.

In 1945, Kety and Schmidt1 devised a method to measure cerebral blood flow using a diffusible indicator, nitrous oxide. In 1949, Kety2 substituted 24Na and described the first practical method to measure blood flow using a radionuclide tracer. In the following years, some groups3–11 elaborated further on Kety’s work and developed methods for measuring myocardial blood flow by injection of diffusible tracers into a coronary artery or into the myocardium itself. The disappearance, or “washout,” of radioactivity was measured by an external radiation-detection system placed over the myocardium. Kety had shown that the rate of washout of the diffusible indicator from tissue to blood was a function of tissue blood flow.1,2,12

The clinical course and coronary arteriographic findings in eight patients with Prinzmetal's variant angina pectoris are reviewed and contrasted to previously reported cases. In six patients with S-T-elevation inferiorly, three had normal coronary arteriograms, one had complete right coronary artery occlusion, one had diffuse triple-vessel disease, and one did not undergo coronary arteriography. In two patients with S-T-elevation anteriorly, severe stenosis of the anterior descending coronary artery was present. Medical treatment in four patients and surgical revascularization of the anterior descending coronary artery in two patients were both accompanied by marked symptomatic improvement. Spontaneous loss of angina occurred in two patients. During 17 months' mean follow-up, seven patients have remained free of angina and one died suddenly. Variant angina pectoris may be accompanied by a variety of coronary arteriographic findings and the prognosis appears more favorable than previously reported.

The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis. When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.

"Ischemic" electrocardiographic changes are frequently associated with a mid-systolic click and late systolic murmur. Neither the cause of these electrocardiographic changes nor the natural history of patients with this syndrome has been determined. Five patients with the auscultatory findings of the "mitral click syndrome," as well as "ischemic" electrocardiographic changes, were studied because coronary-artery anomalies or disease was suspected. Phonocardiograms were obtained with patient supine and upright, and during amyl nitrite inhalation, Valsalva maneuver and phasic respiration. Four of five graded bicycle exercise tests were normal, and there were no arrhythmias. At catheterization, prolapsed posterior-mitral-valve leaflets and normal coronary arteriograms were found in all five patients. Repeat catheterizations in two patients spanning five and eight years revealed mild progression in severity of the mitral-valve prolapse. In patients with mitral-valve prolapse the associated "ischemic"...

The influence of a relatively small increase in serum osmolality produced by hypertonic mannitol on ventricular and systemic arterial hemodynamics and coronary blood flow was studied in 20 patients undergoing cardiac catheterization. Mannitol given to increase serum osmolality 10 mOsm resulted in a small but significant increase in mean systemic arterial pressure, maximum LV dp/dt, left ventricular end-diastolic pressure and cardiac output but no significant change in heart rate or hematocrit. The most prominent change in the patients studied, however, was in coronary blood flow which increased 39% after mannitol. Patients with severe two and three vessel coronary artery disease had increased in coronary blood flow similar to those in patients without coronary artery disease. The data suggest the need to further evaluate the physiological importance of the increase in coronary blood flow produced by mannitol in patients with coronary artery disease and indicate the possibility that mannitol might be of value in treating certain problems in patients with coronary artery disease

Scintillation scanning of the placenta with technetium Tc 99m serum albumin is advanced as an excellent diagnostic technique for safely localizing placental sites in abdominal pregnancy.