Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction

To assess various factors associated with anterior S-T segment depression during acute inferior myocardial infarction, 47 consecutive patients with electrocardiographic evidence of a first transmural inferior infarction were studied prospectively with radionuclide ventriculography an average of 7.3 hours (range 2.9 to 15.3) after the onset of symptoms. Thirty-nine patients (Group I) had anterior S-T depression in the initial electrocardiogram and 8 (Group II) did not have such “reciprocal” changes. There was no difference between the two groups in left ventricular end-diastolic or end-systolic volume index or left ventricular ejection fraction. Stroke volume index was greater in Group I than in Group II. There were no group differences in left ventricular total or regional wall motion scores. A weak correlation existed between the quantities (mV) of inferior S-T segment elevation and reciprocal S-T depression. No relation between anterior S-T segment depression and the left ventricular end-diastolic volume index could be demonstrated; the extent of left ventricular apical and right ventricular wall motion abnormalities, both frequently associated with inferior infarction, did not correlate with the quantity of anterior S-T depression.These data show that anterior S-T segment depression occurs commonly during the early evolution of transmural inferior infarction, is not generally a marker of functionally significant anterior ischemia and cannot be used to predict left ventricular function in individual patients. Anterior S-T segment depression may be determined by reciprocal mechanisms.     

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. III. Influence of basal heart rate

The influence of basal heart rate (HR) on the effects of inotropic (dobutamine infusion) and chronotropic (atrial pacing) stimuli during acute myocardial ischemia was assessed by measurement of intramural carbon dioxide partial pressure (PCO2) in open-chest dogs undergoing transient 10-minute left anterior descending coronary artery occlusions. In protocol I, in 5 dogs anesthetized with pentobarbital alone, HR increased from 153 +/- 10 to 182 +/- 7 beats/min between experimental coronary occlusions, but the increase in ischemic zone intramural carbon dioxide tension (delta PmCO2) was not altered by this significant increase in HR. In protocols II to V, dogs were anesthetized with combinations of morphine, thiamylal and pentobarbital and had a basal average HR of 81 beats/min. Atrial pacing in protocol II (13 dogs) increased HR from 76 +/- 21 to 134 +/- 19 beats/min (p less than 0.001); left ventricular (LV) myocardial oxygen consumption (MVO2) rose from 3.9 +/- 1.6 to 4.9 +/- 1.4 ml/min/100 g (p less than 0.05), and delta PmCO2 rose from 42 +/- 14 to 50 +/- 15 mm Hg (p less than 0.01), indicating more severe ischemic injury during the second experimental coronary occlusion. In protocol III, 11 dogs received 20 micrograms/kg/min of dobutamine before the second experimental occlusion, which significantly (p less than 0.02) increased HR, LV dP/dt and MVO2; delta PmCO2 increased from 46 +/- 13 to 63 +/- 18 mm Hg (p less than 0.01). The 7 dogs in protocol IV received 3.9 +/- 1.9 micrograms/kg/min of dobutamine, titrated such that HR was unchanged (84 +/- 10 vs 81 +/- 15 beats/min), but LV dP/dt increased by 92% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Permanent pacing in patients with transient trifascicular block during acute myocardial infarction

Patients with acute myocardial infarction and transient complete atrioventricular (A-V) block in association with right bundle branch block and left anterior hemiblock have a high incidence rate of late sudden death presumably due to recurrent A-V block. Over a 5 year period, 18 patients demonstrated right bundle branch block and left anterior hemiblock and had transient complete block during an acute myocardial infarction and survived to hospital discharge. Of six patients who did not have permanent pacing, five died suddenly (one was lost to follow-up) with a mean survival time of 2.4 months after hospital discharge. Twelve subsequent patients received permanent demand pacemakers and had a significantly improved prognosis with a mean survival time of 18 months (P < 0.001). Six patients were still alive at an average follow-up time of 20 months. Prophylactic permanent pacing significantly improves the prognosis after acute myocardial infarction in this select subgroup of patients.     

Value of radionuclide ventriculography in the immediate characterization of patients with acute myocardial infarction

The ability of admission radionuclide ventriculography to discriminate among various clinical subsets was evaluated in patients with acute myocardial infarction. One hundred patients with acute myocardial infarction were evaluated within 8 ± 3.1 hours (mean ± standard deviation) after the onset of chest pain. Forty-one patients were in Killip functional class I, 52 in class II and 7 in class III. The mean radionuclide left ventricular ejection fraction was significantly lower in patients with higher Killip classification because of significant elevation of mean left ventricular end-systolic volume rather than significantly altered mean end-diastolic volume. Killip classification frequently failed to correlate with ejection fraction in individual cases. Admission chest X-ray findings were categorized according to the presence of findings suggestive of impaired left ventricular function. Mean left ventricular ejection fraction was significantly lower in patients with abnormal than in patients with normal chest X-ray findings because of significant elevations in both mean end-diastolic and end-systolic volumes. The chest X-ray findings frequently failed to correlate with ejection fraction in individual cases.Stepwise linear regression analysis was employed to analyze the ability of historical, physical, electrocardiographic and chest X-ray findings to predict radionuclide left ventricular ejection fraction. The most predictive variables in order of decreasing significance were anterior myocardial infarction, abnormal chest X-ray findings, rales to two thirds of the posterior thorax, previous myocardial infarction, transmural myocardial infarction and heart rate greater than 100 beats/min. However, even these six optimal predictive variables could explain only 42 percent of the observed variability in left ventricular ejection fraction. Thus, early radionuclide ventriculography adds significantly to the discriminant power of clinical and radiographic characterization of ventricular function in patients with acute myocardial infarction.     

Effects of fluorocarbons with and without oxygen supplementation on cardiac hemodynamics and energetics

Because of uncertainty about the mechanism by which fluorocarbons ameliorate myocardial ischemia, the effects of a fluorocarbon emulsion, perfluorodecalin and perfluorotripropylamine (Fluosol-DA 20% TM) with and without 100% O2 inhalation, on cardiac hemodynamics and energetics were studied in the anesthetized dog. Left ventricular (LV) intramural partial pressure of oxygen (PmO2) was measured by mass spectrometry before and after intravenous infusion of Fluosol-DA 20% (40 ml/kg), and was compared with measurements made in another group of dogs receiving the volume expander dextran (36 ml/kg). Both groups of dogs were then ventilated with 100% O2 and repeat measurements were performed. In the 11 animals receiving fluorocarbons, there were increases in left atrial pressure, LV myocardial blood flow, and LV myocardial O2 consumption (MVO2) compatible with volume expansion. After 100% O2, LV MVO2 decreased to control values, while PmO2 increased to 127 +/- 48 mm Hg (p less than 0.001). There were no significant changes in heart rate, arterial pressure or first derivative of LV pressure (dP/dt) during the study. In 10 dogs treated with dextran there was no change in heart rate or dP/dt, but arterial and left atrial pressures were higher after dextran infusion and remained elevated after 100% O2 inhalation. LV MVO2 increased with volume expansion, and remained increased after 100% O2. PmO2 (66 +/- 18 mm Hg) after 100% O2 was lower (p less than 0.02) than in the fluorocarbon-treated dogs after O2 inhalation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early detection of left ventricular dysfunction in chronic aortic regurgitation as assessed by contrast angiography, echocardiography, and rest and exercise scintigraphy

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/m², (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/m², 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.     

Measurement of aortic root size by biplane angiography before cardiac valve replacement

Aortic valve replacement (AVR) in the patient with a small aortic root demands special consideration because the hemodynamic function of artificial valves with a small external diameter is often poor. In this study, the internal diameter of the aortic root was measured from biplane ventriculography. This measured root diameter was then used to predict the external diameter of the artificial valve. Twelve patients underwent biplane ventriculography followed by AVR with Carpentier-Edwards bioprostheses. The artificial valve diameter was predicted with a correlation coefficient of 0.93, a standard error of estimate of 0.89 mm, and an average absolute difference between preoperative measurement and valve diameter of 0.69 mm. Therefore, the aortic root diameter can be accurately measured from the ventriculogram, thus detecting the patient with a small aortic root before surgery.     

Measurement of infarct size in acute canine myocardial infarction by single-photon emission computed tomography with technetium-99m pyrophosphate

The location and extent of myocardial infarction (MI) are important predictors of patient course. The current study tests the hypothesis that MI size could be measured accurately using rotating gamma camera single-photon emission computed tomography ( SPECT ) and technetium-99m pyrophosphate (PPi) and that the accuracy of these measurements was independent of MI location and transmural or nontransmural distribution. SPECT was performed in 38 dogs 48 hours after ligation of the left anterior descending coronary artery (14 dogs) or left circumflex coronary artery (LC) (24 dogs) at the mid-level or below. Projection images were corrected for center-of-rotation and field nonuniformity and processed with a 1-dimensional low-pass filter to diminish rib activity. Sixteen 0.5-cm-thick transverse sections, including the entire left ventricle, were reconstructed by filtered backprojection , low-pass filtered, contrast enhanced and processed with a 3-dimensional boundary enhancement operator. The boundary of PPi uptake in each slice was marked automatically using an algorithm that combined a directional derivative and a threshold, and required continuity of the boundary in 3 dimensions. The total number of volume elements that showed abnormal tracer uptake were summed, corrected to absolute volume, and multiplied by the specific weight of cardiac muscle. Scintigraphic MI weight was compared with pathologic MI weight. There was an excellent correlation between scintigraphic and pathologic MI weight. The poorer correlation for nontransmural compared with transmural MIs is most likely a function of size alone, since MIs that weighed less than 10 g (n = 12, range 1.3 to 9.5 g), both transmural and nontransmural, showed a similar correlation: S = 1.07 X P + 0.56 (r = 0.81, standard error of the slope = 0.245).(ABSTRACT TRUNCATED AT 250 WORDS)     

High dose intravenous streptokinase for acute myocardial infarction: preliminary results of a multicenter trial

To assess the efficacy of intravenous streptokinase in patients with acute myocardial infarction, 40 patients (30 men and 10 women, mean age 54 years) with acute myocardial infarction were given 1.5 million U of streptokinase intravenously in 1 hour, and coronary arteriography was performed repeatedly to assess reperfusion. Streptokinase treatment was begun 270 +/- 86 (mean +/- SD) minutes after the onset of chest pain. Of the 40 patients, 34 had total or near total coronary occlusion before streptokinase administration. In 14 (41%) of these 34 patients, some reperfusion occurred during the 90 minutes after the administration of streptokinase, but in only 11 of the 14 was reperfusion present at 90 minutes. After streptokinase administration, all patients received heparin for 8 to 10 days; they were subsequently administered aspirin and dipyridamole. Clinical evidence of reocclusion during the first 24 hours of heparin therapy occurred in one patient. Thus, when given to patients with acute myocardial infarction and total coronary occlusion an average of 4 1/2 hours after the onset of chest pain, high dose intravenous streptokinase achieves reperfusion in only about 40% and results in sustained reperfusion in only about 30%.     

Nongeometric determination of right ventricular volumes from equilibrium blood pool scans

It has previously been shown that left ventricular volumes can be measured accurately from radionuclide gated blood pool scintigrams by quantttating the background-corrected and volume-normalized ventricular activity at end-diastole and end-systole. To determine if this same technique can be applied to the calculation of right ventricular volumes, simultaneous measurements of right ventricular stroke volume were performed using gated scintigraphy and the thermodilution technique in 60 patients without clinical or hemodynamic evidence of right-sided regurgitation. Three techniques for the acquisition of the radionuclide studies were evaluated. The best correlation between scintigraphic and thermodilution determinations of stroke volume was obtained for studies acquired with a 25 ° rotating slant hole collimator positioned in a 10 to 15 ° left anterior oblique projection with the collimator slant directed toward the cardiac apex along the axis of the interventricular septum: Thermodilution stroke volume = 4.2 (scintigraphic stroke volume) + 10.3 ml (correlation coefficient [r] = 0.88; standard error of the estimate = 9.3 ml; probability [p] < 0.0001). This scintigraphic acquisition technique was superior to (1) a straight bore collimator positioned in a septal projection (30 to 50 ° left anterior oblique with 15 ° caudal tilt), and (2) a 25 ° slant hole collimator positioned in a similar septal projection with the collimator slant directed caudally. This method was evaluated prospectively in an additional 14 patients, and there was excellent agreement between stroke volumes obtained with thermodilution and scintigraphic methods (r = 0.96, p < 0.001). In addition, measurements of right ventricular ejection fraction by the equilibrium method agreed closely with those obtained with a gated first pass technique (r = 0.94, p < 0.001, n = 14). With use of the scintigraphic right ventricular ejection fraction and the relation between scintigraphic and thermodilution measurements of right ventricular stroke volume, right ventricular end-diastolic and end-systolic volumes can be estimated. Thus, nongeometric radionuclide techniques may be used for the quantitation of right ventricular volumes.     

Left ventricular volumes by single-plane cineangiography: in vivo validation of the Kennedy regression equation

This study was performed to assess the accuracy and reliability of the regression equations of Kennedy et al and Wynne et al in the quantitation of single plane left ventricular (LV) volumes. In 15 patients with normal LV function and without intracardiac shunting or valvular insufficiency, gated equilibrium blood pool scintigraphy was performed simultaneously with the measurement of cardiac output (by thermodilution), after which left ventriculography was performed in the 30 degrees right anterior oblique (RAO) projection. From the scintigraphically determined LV ejection fraction (EF) and the thermodilution-measured stroke volume (SV), absolute LV volumes were calculated. The cineangiographic LV volumes obtained with the regression equation of Kennedy et al closely approximated those calculated by scintigraphy/thermodilution, whereas the volumes determined using the regression equation of Wynne et al were larger (p less than 0.05) than the calculated volumes. In 204 patients without intracardiac shunting or valvular insufficiency, SV was measured by the Fick or indicator dilution methods, after which single-plane left ventriculography was performed in the 30 degrees RAO projection. In the 83 patients without coronary artery disease with normal (n = 69) or depressed (n = 14) LVEF, cineangiographic SV (obtained using the regression equation of Kennedy et al) closely approximated forward SV. Similarly, this relation was excellent in the 142 patients whose LVEFs were greater than or equal to 0.50.(ABSTRACT TRUNCATED AT 250 WORDS)     

Iodine-123 phenylpentadecanoic acid: Detection of acute myocardial infarction and injury in dogs using an iodinated fatty acid and single-photon emission tomography

The ability of an iodinated fatty acid, iodine-123 Phenylpentadecanoic acid (1–123 PPA), and single-photon emission computed tomography (SPECT) to detect myocardium injured by temporary or permanent coronary arterial occlusion was evaluated. In 5 control dogs, 11 dogs that underwent 90 to 120 minutes of fixed left anterior descending coronary artery (LAD) occlusion, and 8 dogs that underwent 90 minutes of temporary LAD occlusion and up to 90 minutes of reflow, 2 to 6 mCi of 1–123 PPA were injected and the dogs were imaged with SPECT. Control dogs showed relatively uniform uptake and clearance of 1–123 PPA in similar left ventricular (LV) regions. Dogs with permanent LAD occlusion were identified by computer algorithm as having regions of decreased 1–123 PPA uptake in the infarct-related area and a reduced rate of 1–123 PPA clearance (−9.4% in infarct sectors [washin], +3.7% in sectors adjacent to the area of infarction, and +15.4% in control LV sectors [p <0.01]). Dogs with temporary LAD occlusion and reperfusion had decreased clearance of 1–123 PPA from the regions with infarction; 1–123 PPA clearance was −5.2 ± 16.4% in infarct sectors, 12.7 ± 7.4% in periinfarct zones, and 30.4 ± 12% in control LV regions. These data demonstrate that tomographic analysis of 1–123 PPA uptake and clearance permits the relatively noninvasive detection of LV myocardium injured by permanent or temporary LAD occlusion and reperfusion.     

Myocardial rupture after myocardial infarction: Detection by multi-gated image-acquisition scintigraphy

Myocardial rupture following infarction usually is an acute and dramatic event. Rarely, it may take a subacute course, allowing surgical treatment. We report herein a case of subacute rupture of the heart in a 54 year old patient with acute myocardial infarction. The rupture was diagnosed by the appearance of a radiopaque halo around the heart during radionuclide ventriculography. The patient subsequently underwent surgical resection of a large anterolateral aneurysm and a 2 inch long rupture of the myocardium and survived. Clinical suspicion, prompt diagnosis, and surgical intervention are important in the management of this relatively unusual complication of infarction.     

Prognostic value of submaximal exercise radionuclide ventriculography after myocardial infarction

Submaximal exercise testing with radionuclide ventriculography (RVG) was performed in 117 patients before hospital discharge 17 +/- 7 days (+/- standard deviation) after an acute myocardial infarction (MI). The hypothesis tested in these studies was that submaximal exercise testing coupled to RVG allows the identification of patients at risk for future ischemic events in the subsequent 6 months, irrespective of MI location and type. The sites of MI were characterized as anterior transmural in 33, inferior transmural in 39, limited nontransmural in 18, extensive nontransmural in 24 and indeterminant in 3. During 6 months of follow-up, 9 patients died, 14 had recurrent MI, 18 had refractory angina pectoris, 16 had limiting angina and 17 had congestive heart failure. Discriminant function analysis ranked exercise changes in left ventricular (LV) ejection fraction and end-systolic volume the most important of all clinical, exercise and scintigraphic variables for predicting future cardiac events. The predictive accuracy of changes in LV ejection fraction and end-systolic volume were 93 and 91%, respectively, for the entire group, and were significantly more sensitive than any degree of ST-segment depression or elevation (p less than 0.001). These findings were generally independent of MI location and type. Thus, submaximal exercise RVG after MI is an accurate means of identifying patients at risk for major cardiac events in the 6 months after hospital discharge.     

ST isopotential precordial surface maps in patients with acute myocardial infarction.

ST amplitude distributions were studied in 41 patients with acute myocardial infarction by deriving isopotential maps from a 5 x 7 electrode precordial matrix. Independent data on infarct size and localization were obtained utilizing the technetium 99m stannous pyrophosphate scintigraphic method. The locus of maximal ST elevation was stable for at least two days in 86% of 27 patients with anterior infarction. A single maximum or maximum-minimum was found in 88% but 22% of the patients had multiple maxima and/or minima in at least two maps. Areas of significant ST elevation were often excluded from the precordial matrix. The site of maximal ST elevation correlated with scintigraphic infarct site but was displaced medially in lateral infarction. The relation between infarct size and sigmaST elevation was significant and curvilinear. sigmaST underestimated size in large anterior infarction. The correlation of the size and the number of sites with ST elevation greater than or equal to 1.5 mm was weak (r = 0.56). The degree of ST abnormality in 14 patients with inferior infarction decreased significantly during the initial 24 hours. The isopotential maps were similar to those obtained in anterior infarction but the polarity was reversed. The results provide limited support for the continued exploration of ST analysis as a clinical method but suggest that sizing methods should be based on total body surface mapping, taking into account the geometry and electrical properties of the torso.     

Alterations in left ventricular volumes and ejection fraction at rest and during exercise in patients with aortic regurgitation

This study was performed (1) to determine the changes in left ventricular volumes during exercise in patients with aortic regurgitation, and (2) to evaluate the importance of these alterations in characterizing left ventricular function in these patients. In 15 normal subjects (Group I) and in 17 patients with aortic regurgitation (Group II), left ventricular end-diastolic volume index, end-systolic volume index, ejection fraction and the ratio of peak systolic blood pressure to end-systolic volume index were measured at rest and during supine exercise. The patients with aortic regurgitation were classified into two groups on the basis of symptoms and chest radiographs: Group IIA, minimal or no symptoms, no cardiomegaly or pulmonary venous congestion; Group IIB, definite symptoms, with cardiomegaly and pulmonary venous congestion. Patients with aortic regurgitation had greater left ventricular end-diastolic and end-systolic volume indexes at rest and during exercise (p <0.05) than did normal subjects. During exercise, left ventricular end-diastolic volume index increased in normal subjects (53 ± 13 ml/m² [mean ± standard deviation] at rest, 67 ± 18 ml/m² during exercise, p <0.01), demonstrated a heterogeneous response in patients in Group IIA and increased in patients in Group IIB (180 ± 96 ml/m² at rest, 209 ± 102 ml/m² during exercise, p <0.05). During exercise, left ventricular end-systolic volume index decreased in normal subjects (18 ± 5 ml/m² at rest, $\text{15}\text{\$}\text{?}\text{6}$ ml/m² with exercise, p <0.01), increased in patients in Group IIB (82 ± 60 ml/m² at rest, 118 ± 93 ml/m² during exercise, p <0.05), and showed a variable response in those in Group IIA. At rest, left ventricular ejection fraction was similar in the three groups, but during exercise it increased in Group I (0.71 ± 0.07 at rest, 0.82 ± 0.07 with exercise, p <0.001), was unchanged in Group IIA and decreased in Group IIB (0.59 ± 0.15 at rest, 0.50 ± 0.16 during exercise, p <0.05). During exercise, there was an inverse relation between changes in left ventricular ejection fraction and endsystolic volume, but no relation between changes in end-diastolic volume and ejection fraction. Changes in the systolic pressure-volume ratio provided no more information than changes in end-systolic volume alone. Thus, abnormal alterations in left ventricular volumes occur during exercise in patients with aortic regurgitation and may be helpful in the further characterization of left ventricular performance in these patients.     

Determination of left ventricular mass by single-photon emission computed tomography with thallium-201

To test the hypothesis that single-photon emission computed tomography (SPECT) might permit accurate, noninvasive measurement of LV mass, SPECT measurements of LV mass to LV weight were compared in 20 mongrel dogs. Projection images of the left ventricle were acquired after intravenous injection of thallium-201 (TI-201). Transverse sections were reconstructed using filtered backprojection. Coronal sections were extracted from the reconstructed volume. The boundary of LV uptake of TI-201 in each coronal section was defined automatically using a threshold detector. Scintigraphic LV mass [total number of volume elements (voxels) showing TI-201 uptake X voxel volume X specific gravity of myocardium] was compared to actual LV weight. There was good correlation between scintigraphic LV mass and LV weight. Mean LV weight was 68 +/- 20 g (+/- standard deviation) (range 27 to 94). Mean SPECT LV mass was 66 +/- 19 g (range 28 to 100). Linear regression analysis yielded the following relation: SPECT LV mass = 0.87 X LV weight + 6.79 (r = 0.91, root-mean-square deviation from regression = 7.5). SPECT measurements were reproducible, with a coefficient of variation of 0.24%. Thus, SPECT of LV TI-201 distribution can be used to measure LV mass in canine myocardium.     

Clinicopathologic correlates of acute ischemic heart disease syndromes

To better define the relations among acute and chronic coronary arterial lesions and different syndromes of acute ischemic heart disease, the clinicopathologic findings in 100 recent myocardial infarcts in 83 patients were reviewed and the results correlated with those of previous studies. Severe atherosclerosis (greater than 75 percent narrowing of luminal cross-sectional area) involved three or more major coronary arteries in 65 percent; two arteries in 16 percent, one artery in 15 percent, and no arteries in 4 percent of cases. The incidence rate of recent occlusive coronary arterial lesions was 61 percent, including 50 (90.2 percent) of 55 grossly apparent transmural infarcts, 9 (34.6 percent) of 26 grossly evident subendocardial infarcts and 2 (10.5 percent) of 19 multifocal microinfarcts associated with clinical episodes of acute coronary insufficiency (p <0.001). The 61 recent occlusive lesions consisted of two thromboemboli, two isolated plaque hemorrhages and 57 in situ thrombi that were associated with a high incidence rate of plaque erosion, rupture and hemorrhage. Clinical conditions predisposing to reduced coronary perfusion were identified before the onset of 26.2 percent of infarcts with recent occlusions and 61.5 percent of infarcts without recent occlusions (p <0.001). Clinical onset of infarction was followed by severe cardiac pump failure or congestive heart failure in 63.9 percent of infarcts with and 41.0 percent of infarcts without recent occlusions (p = 0.04).From this and previous studies, it is concluded that (1) acute ischemic heart disease does not have a constant relation with the severity of chronic atherosclerosis; (2) myocardial necrosis commonly occurs in the absence of acute permanent coronary occlusion, but in this setting is usually limited to subendocardial involvement of variable extent; (3) acute coronary thrombosis frequently acts as a major factor in determining the extent and distribution of an evolving infarct, as indicated by the large incidence of occlusive coronary thrombi with regional transmural infarcts; and (4) coronary thrombus formation is not dependent on a generalized impairment of coronary perfusion, either before or after the onset of infarction.     

Hyperlipoproteinemia: metabolic basis and rationale for therapy

Most forms of hyperlipoproteinemia are the result of at least 1 to 4 basic defects of lipoprotein metabolism. Hypercholesterolemia is most commonly due to decreased activity of receptors for low-density lipoproteins (LDL). A deficiency of LDL receptors can be caused by either a genetic defect in the structure of the receptor or metabolic suppression of receptor synthesis by genetic factors or dietary saturated fatty acids and cholesterol. An elevation of triglycerides in chylomicrons or very low density lipoproteins (VLDL) can be secondary to a reduced activity of lipoprotein lipase, and an increase in the catabolic remnants of these lipoproteins can be due to an abnormal isoform of apolipoprotein E, the apolipoprotein that mediates hepatic uptake of lipoprotein remnants. Finally, hepatic overproduction of VLDL can produce hypertriglyceridemia, or if there is a concomitant defect in clearance of lipoproteins, an accentuated increase of VLDL, remnants or LDL will occur. Thus, lipoprotein overproduction can give rise to multiple lipoprotein phenotypes in a single family. Specific therapy of hyperlipoproteinemia should be directed toward correcting these metabolic defects.