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Biomedical subjects

M Dae

Publications and source records attributed to M Dae.

At least 19 recordsLinked to original sources

Buspirone and meperidine synergistically reduce the shivering threshold.

UNLABELLED: Mild hypothermia (i.e., 34 degrees C) may prove therapeutic for patients with stroke, but it usually provokes shivering. We tested the hypothesis that the combination of buspirone (a serotonin 1A partial agonist) and meperidine synergistically reduces the shivering threshold (triggering tympanic membrane temperature) to at least 34 degrees C while producing little sedation or respiratory depression. Eight volunteers each participated on four randomly-assigned days: 1) large-dose oral buspirone (60 mg); 2) large-dose IV meperidine (target plasma concentration of 0.8 microg/mL); 3) the combination of buspirone (30 mg) and meperidine (0.4 microg/mL); and 4) a control day without drugs. Core hypothermia was induced by infusion of lactated Ringer's solution at 4 degrees C. The control shivering threshold was 35.7 degrees C +/- 0.2 degrees C. The threshold was 35.0 degrees C +/- 0.8 degrees C during large-dose buspirone and 33.4 degrees C +/- 0.3 degrees C during large-dose meperidine. The threshold during the combination of the two drugs was 33.4 degrees C +/- 0.7 degrees C. There was minimal sedation on the buspirone and combination days and mild sedation on the large-dose meperidine day. End-tidal PCO2 increased approximately 10 mm Hg with meperidine alone. Buspirone alone slightly reduced the shivering threshold. The combination of small-dose buspirone and small-dose meperidine acted synergistically to reduce the shivering threshold while causing little sedation or respiratory toxicity. IMPLICATIONS: Mild hypothermia may be an effective treatment for acute stroke, but it usually triggers shivering, which could be harmful. Our results indicate that the combination of small-dose buspirone and small-dose meperidine acts synergistically to reduce the shivering threshold while causing little sedation or respiratory toxicity. This combination may facilitate the induction of therapeutic hypothermia in stroke victims.

Adult↗

Heterogeneous sympathetic innervation influences local myocardial repolarization in normally perfused rabbit hearts.

BACKGROUND: Heterogeneity of sympathetic innervation is thought to contribute to the potential for fatal arrhythmia. However, little is known about the effects of heterogeneous innervation on repolarization. METHODS AND RESULTS: To assess this relationship, we measured activation recovery intervals (ARIs) from 64 epicardial sites in 11 rabbits studied 2 weeks after regional denervation produced by phenol and 4 sham-operated rabbits. ARI results were compared with the distribution of sympathetic innervation measured from 3D reconstructions of serial autoradiographs of [(125)I]metaiodobenzylguanidine and (99m)Tc-sestamibi. ARIs were recorded during baseline sinus rhythm, norepinephrine (NE) infusion (0.1 microg. kg(-1). min(-1)), and left stellate ganglion stimulation (SS). NE shortened ARI in 98% of electrodes in the denervated region. The degree of ARI shortening and dispersion increased (P<0.001 and P<0.01, respectively) as denervation became more severe. SS shortened ARI in 30% of electrodes in the denervated area, with increased shortening and dispersion related to increased severity of denervation (P<0.01). SS prolonged ARI in 70% of electrodes in the denervated area, with no correlation with severity of denervation. CONCLUSIONS: The magnitude and dispersion of local repolarization responses are related to the severity of denervation, as well as the type of stimulation: neural (SS) versus humoral (NE). The differences may relate to the concentration of NE released.

3-Iodobenzylguanidine↗

Iodine-123 metaiodobenzylguanidine scintigraphic assessment of the transplanted human heart: evidence for late reinnervation.

OBJECTIVES: This study attempted to determine whether cardiac sympathetic reinnervation occurs late after orthotopic heart transplantation. BACKGROUND: Metaiodobenzylguanidine (MIBG) is taken up by myocardial sympathetic nerves. Iodine-123 (I-123) MIBG cardiac uptake reflects intact myocardial sympathetic innervation of the heart. Cardiac transplant recipients do not demonstrate I-123 MIBG cardiac uptake when studied < 6 months from transplantation. However, physiologic and biochemical studies suggest that sympathetic reinnervation of the heart can occur > 1 year after transplantation. METHODS: We performed serial cardiac I-123 MIBG imaging in 23 cardiac transplant recipients early (< or = 1 year) and late (> 1 year) after operation. In 16 subjects transmyocardial norepinephrine release was measured late after transplantation. RESULTS: No subject had visible I-123 MIBG uptake on imaging < 1 year after transplantation. However, 11 (48%) of 23 subjects developed visible cardiac I-123 MIBG uptake 1 to 2 years after transplantation. Only 3 (25%) of 12 subjects with a pretransplantation diagnosis of idiopathic cardiomyopathy demonstrated I-123 MIBG uptake compared with 8 (73%) of 11 with a pretransplantation diagnosis of ischemic or rheumatic heart disease (p = 0.04). All 10 subjects with a net myocardial release of norepinephrine had cardiac I-123 MIBG uptake; all 6 subjects without a net release of norepinephrine had no cardiac I-123 MIBG uptake. CONCLUSIONS: Sympathetic reinnervation of the transplanted human heart can occur > 1 year after operation, as assessed by I-123 MIBG imaging and the transmyocardial release of norepinephrine. Reinnervation is less likely to occur in patients with a pretransplantation diagnosis of idiopathic cardiomyopathy than in those with other etiologies of congestive heart failure.

3-Iodobenzylguanidine↗

Segmental analysis of resting echocardiographic function and stress scintigraphic perfusion: implications for myocardial viability.

In 73 patients with coronary artery disease, we performed segmental analysis of resting two-dimensional echocardiography and stress thallium-201 single photon emission computed tomographic scintigraphy with 24-hour delayed imaging to test the hypotheses that (1) combined analysis of stress thallium-201 scintigraphy (with 24-hour redistribution) and echocardiography provides an evaluation of the viability of most myocardial segments; and (2) the severity of the scintigraphic perfusion abnormality in a given segment is equivalent to the severity of its echocardiographically determined functional impairment. Scintigraphy showed 14% of the 1168 segments analyzed to have fixed severe defects. Echocardiography showed 11% of the 1070 segments analyzed to be akinetic or dyskinetic. However, with combined analysis, only 62 (5%) segments showed no evidence of viability by either imaging technique. We conclude that in this group of patients, 95% of segments have evidence of viability by one of these two conventional imaging techniques.

Aged↗

Effects of canine myocardial infarction on sympathetic efferent neuronal function: scintigraphic and electrophysiologic correlates.

We studied the effects of nondecentralized left stellate ganglion stimulation on regional epicardial monophasic action potential duration at 50% (APD50) and 90% (APD90) repolarization from 104 sites in 10 surviving dogs with a chronic myocardial infarction model. These effects were correlated with thallium-201 and iodine-123 metiodobenzylguanidine (MIBG) imaging to identify areas of viable but denervated myocardium. Mean infarct size was 5.2% +/- 0.8% total heart weight, and the planimetered areas of denervation were always larger (18% +/- 4% total heart area). During constant ventricular pacing, stellate stimulation tended to shorten the APD90 only in normally innervated areas (364 +/- 5 to 358 +/- 5 msec) and to increase in denervated areas (358 +/- 5 to 362 +/- 5 msec), (p value not significant (NS) for prestellate and poststellate stimulation; p < 0.05 for difference between denervated vs innervated). The APD50 significantly shortened in innervated areas from 287 +/- 5 to 270 +/- 3 msec (p < 0.05) compared with denervated areas (283 +/- 4 to 274 +/- 5 msec, p = NS). We conclude that MIBG imaging demonstration of denervation identifies areas with impaired shortening of the epicardial APD50 in response to stellate stimulation and that nontransmural myocardial infarction produces areas of denervation larger than areas of necrosis.

Action Potentials↗

The scintigraphic characteristics of ventricular pre-excitation through Mahaim fibers with the use of phase analysis.

The phase image pattern of blood pool scintigrams was blindly assessed in 11 patients exhibiting conduction through Mahaim pathways, including 6 nodoventricular and 5 fasciculoventricular. These patterns were compared with the phase image findings in normal subjects, patients with left and right bundle branch block in the absence of pre-excitation and patients with pre-excitation through atrioventricular (AV) connections. In all patients with a Mahaim pathway, the site of earliest phase angle was septal or paraseptal. Phase progression was asymmetric and the pre-excited ventricle demonstrated the earliest mean ventricular phase angle in 10 of 11 patients. This pattern, and the associated ventricular phase difference, appeared to vary from that in normal subjects and in those with a septal AV connection, in whom phase progression is generally symmetric. Scintigraphic phase analysis provided localizing information and presented patterns consistent with Mahaim pathways. Although not able to differentiate among Mahaim pathway subtypes, these phase patterns differed from those in normal subjects, those with right and left lateral free wall pathways and most patients with a septal AV pathway. However, the phase pattern of patients with a Mahaim pathway may not differ from that of patients with a septal AV connection displaying an asymmetric pattern of phase progression, or those with left and right bundle branch block in the absence of pre-excitation. Objective, yet imperfect phase measurements supported these differences. Such image findings may complement the often complex electrophysiologic evaluation of patients presenting with pre-excitation.

Adult↗

ECG left anterior fascicular block reveals diverse patterns on scintigraphic phase analysis.

Left anterior fascicular block (LAFB) remains an uncertain diagnosis by scalar ECG, particularly with coexisting inferior infarction. To assess the use of phase analysis in LAFB, left ventricular phase and amplitude maps were evaluated in the 70-degree left anterior oblique projection in eight control patients and 13 patients with LAFB who met the ECG criteria of Warner et al. The left ventricular region was divided into anterior (A) and inferior (I) segments. Contraction patterns were assessed by examination of the sequence of phase angles (phi), relative contraction time of the anterior versus inferior segments was assessed from the difference between segment mean phase angles, delta phi A-I, determined from the phase histogram, and duration of contraction was assessed by histogram width. Relative stroke volume was assessed on the amplitude image. Eight control subjects had normal amplitude, contraction of the anterior before inferior segment, narrow histogram width, and a normal ECG. Among the 13 patients with ECG LAFB, seven were concordant, with phase analysis demonstrating anterior contraction delay. Two of seven patients had narrow histograms and normal amplitude, which were compatible with isolated anterior conduction delay, and five of seven patients had broad histograms and reduced anterior amplitude, compatible with anterior infarction. Phase analysis was discordant with ECG LAFB diagnosis in six patients. All showed contraction of anterior segments before inferior segments as in normal subjects. Four had broad histograms and reduced inferior amplitude, compatible with prior inferior infarction without LAFB, and two had normal phase and amplitude maps. Phase patterns appear characteristic of LAFB with or without associated infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Bundle-Branch Block↗

Neonatal model of heterotopic heart transplantation in pigs.

To investigate the long-term success of heart transplantation in newborn infants who have complex congenital heart disease, we have developed a model of heterotopic heart transplantation in immature pigs. We chose the heterotopic technique because it is simple, does not require cardiopulmonary bypass or heparin, allows for significant size disparity between the recipient and donor hearts, and allows for experimental comparisons between the two hearts. Small newborn piglet hearts are harvested, prepared, and then transplanted into the left chest of larger weanling pigs to augment or substitute for the native left ventricle. Preliminary data from transplants into 49 pigs suggest that the technique is technically possible, the pigs can be immunosuppressed over the long term, and the donor heart can contribute hemodynamically. Experimentally, the model is well designed for the investigation of issues critical for the long-term success of heart transplantation in infants and children, including growth and development, optimal long-term immunosuppression, differences in immunotolerance, and the study of coronary obliterative disease. Clinically, the model has potential applicability in congenital heart anomalies if one native functioning atrium and ventricle are present.

Animals↗

The clinical and pathophysiologic implications of pain, ST abnormalities, and scintigraphic changes induced during dipyridamole infusion: their relationships to the peripheral hemodynamic response.

In order to determine their significance during dipyridamole perfusion scintigraphy, symptomatic, ECG, and scintigraphic findings were related to each other, to the hemodynamic response, and to angiographic findings in 73 consecutive patients having coronary angiography within 3 months of scintigraphy. The group having induced "cardiac" pain differed from the group without induced pain only in their higher incidence of induced ischemic ST changes, the "marked" hemodynamic response, and their lower incidence of an "absent" hemodynamic response (all p less than 0.01). Induced ST depression was found only in patients with coronary disease. In this population, dipyridamole-induced pain was a moderately specific marker and induced ST abnormalities a more highly specific marker for coronary disease. However, both were insensitive for coronary disease diagnosis. If induced pain or ST abnormalities in the presence of significant coronary disease were accepted as indicators of ischemia, then scintigraphic abnormalities appeared to be produced by dipyridamole in roughly equal incidence by ischemic and nonischemic mechanisms. Induced ischemia related frequently to an exaggerated hypotensive response with no change in double product, suggesting its cause to be an induced increase in myocardial oxygen demand. Dipyridamole-induced image defects were noted even in the absence of a peripheral hemodynamic response. This indicates that the peripheral response does not always correlate with its central coronary effect and an absent peripheral hemodynamic response does not necessarily invalidate scintigraphic results.

Angina Pectoris↗

Effect of transmural versus nontransmural myocardial infarction on inducibility of ventricular arrhythmias during sympathetic stimulation in dogs.

Transmural myocardial infarction interrupts sympathetic nerves and denervates viable muscle distal to myocardial infarction. The effect of sympathetic stimulation on responses to programmed ventricular stimulation was studied in dogs without myocardial infarction (Group I: n = 5), with transmural anterior wall myocardial infarction (Group II: n = 6) and with nontransmural anterior wall myocardial infarction (Group III: n = 9). Ventricular effective refractory period during sympathetic stimulation decreased by 16 +/- 18, 1 +/- 2 and 12 +/- 8 ms (mean +/- SD) in viable muscle of the inferoapical left ventricle in Groups I, II and III, respectively, suggesting efferent sympathetic denervation by transmural myocardial infarction only. Sustained ventricular tachycardia or fibrillation was induced more easily during sympathetic stimulation in six of the six dogs with transmural infarction, but in only two of the nine dogs with nontransmural infarction (p less than 0.01). It is concluded that the partial sympathetic denervation produced by transmural myocardial infarction enhances the ease of induction of ventricular tachycardia and fibrillation during sympathetic stimulation. A similar mechanism may lead to increased risk for lethal arrhythmias during periods of high sympathetic tone in patients with transmural myocardial infarction.

Animals↗

Gallium lung scintigraphy in amiodarone pulmonary toxicity.

We sought to assess the role of gallium-67 lung scintigrams in the evaluation of amiodarone pulmonary toxicity. Images and laboratory studies were evaluated in 54 patients who had chest radiographs and scintigraphic studies during amiodarone treatment of more than one month's duration among 561 patients receiving the medication for refractory arrhythmias. There were 22 patients with pulmonary symptoms and clinical evidence of amiodarone pulmonary toxicity (group 1); 19 patients had other causes for pulmonary symptoms (group 2); and 21 patients were without symptoms or other clinical evidence of pulmonary toxicity (group 3). There was no difference among groups in treatment duration or total amiodarone dose. Symptomatic presentation could not differentiate between group 1 and group 2 patients. However, radiographic findings of isolated pulmonary congestion or a normal radiograph in the presence of symptoms made amiodarone toxicity unlikely, while the appearance of new, dense radiographic infiltrates--often in a nodular distribution--were more frequent among group 1 patients (p less than 0.01). During symptomatic periods, 18 of 22 group 1 patients had abnormal gallium lung uptake, while four revealed more subtle serial changes but there was only one abnormal scintigram among symptomatic group 2 patients. Nonspecific radiographic abnormalities in patients with pulmonary symptoms on amiodarone therapy were rarely attributed to toxicity in the presence of a normal scintigram. One group 3 patient developed scintigraphic abnormalities early during amiodarone treatment, suggesting toxicity in the presence of a normal chest x-ray examination. Comparison of radiographic and scintigraphic studies performed during symptoms with those performed prior to symptom development best indicated the diagnosis, while comparison with later images assessed the efficacy of treatment. Diffusion capacity testing and transbronchial biopsy were sensitive but not specific for the diagnosis of amiodarone toxicity. Gallium image abnormalities parallel the development of amiodarone pulmonary toxicity and aid this diagnosis, especially when the chest radiograph is abnormal and ambiguous. Serial increments in scintigraphic abnormality appear especially helpful for diagnosis in the population at risk.

Adult↗

Augmented preexcitation assessed by scintigraphic phase analysis during atrial pacing.

We sought to characterize the effect of augmented preexcitation on the phase image pattern associated with scintigraphic acquisition during conduction via accessory arteriovenous connections. For this reason we assessed phase image scintigraphy, acquired in sinus rhythm and during rapid atrial pacing in 12 patients with documented right (five patients) or left (seven patients) lateral accessory pathways. Augmented preexcitation during atrial pacing was documented at electrophysiologic study in all patients during atrial pacing at similar rates. Phase analysis was abnormal in only 8 patients during sinus rhythm but in all 12 patients during atrial pacing. Atrial pacing brought a significant delay in both mean left and right ventricular phase angles, LV phi and RV phi, respectively. With atrial pacing, the site of earliest phase angle, interpreted to indicate the site of earliest excitation, shifted to the site of the accessory pathway. There was increased relative "prematurity" of the mean phase angle of the ipsilateral ventricle and an absolute increase in the difference between mean and earliest left and right ventricular phase angles, delta phi (LV-RV) and delta phi 0 (LV-RV), respectively. In patients with right-sided pathways, delta phi (LV-RV) increased from 9.5 +/- 12.6 degrees to 47.9 +/- 22.8 degrees, whereas delta phi 0 (LV-RV) increased from 28.1 +/- 18.0 degrees to 67.6 +/- 25.0 degrees (both p less than 0.05). Patients with left-sided pathways demonstrated similar changes in which delta phi (LV-RV) decreased from 2.9 +/- 10.8 degrees to -26.5 +/- 9.0 degrees and delta phi 0 (LV-RV) decreased from 3.4 +/- 14.2 degrees to -27.4 +/- 17.9 degrees (both p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Hemodynamic and clinical evaluation of piroximone, a new inotrope-vasodilator agent, in severe congestive heart failure.

To assess the potential utility of piroximone (MDL-19,205), an investigational inotrope-vasodilator agent, in severe heart failure, 15 patients with severe left ventricular failure refractory to conventional agents were enrolled in an acute hemodynamic study. After incremental intravenous dosing (mean total dose 1.8 +/- 0.4 mg/kg body weight), cardiac index increased (1.7 +/- 0.3 to 2.6 +/- 0.6 liters/min per m2; p less than 0.001) and left ventricular filling pressure decreased (25 +/- 7 to 19 +/- 7 mm Hg; p less than 0.001). Also decreasing significantly were right atrial pressure (13 +/- 6 to 7 +/- 5 mm Hg; p less than 0.005) and systemic vascular resistance (1,633 +/- 394 to 1,183 +/- 278 dynes.s.cm-5; p less than 0.001). Heart rate and mean arterial pressure did not change, whereas stroke work index increased significantly (13.3 +/- 4.3 to 21.6 +/- 7.3 g.m/m2; p less than 0.005). The increase in stroke work index with a concomitant decrease in left ventricular filling pressure indicates an improvement in systolic performance after treatment with piroximone. Similar responses were obtained after incremental doses of piroximone in oral solution. After oral doses of piroximone tablets, cardiac index also increased significantly (2.1 +/- 0.6 to 2.4 +/- 0.5 liters/min per m2; p less than 0.05), although this magnitude of increase was comparatively low. In a subgroup of 10 patients who underwent equilibrium gated radionuclide blood pool scintigraphy before and after intravenous piroximone, end-diastolic volume index tended to increase (106 +/- 42 to 132 +/- 60 ml/m2; p = 0.07), whereas left ventricular filling pressure decreased significantly (26 +/- 8 to 19 +/- 9 mm Hg; p less than 0.01).

Aged↗

Quantitation of mitral regurgitation by Doppler echocardiography.

The evaluation and care of patients with mitral regurgitation would be facilitated by an easy, reproducible and noninvasive method that could quantitate the hemodynamic burden. In this study, we describe a new Doppler echocardiographic method that measures the regurgitant fraction and we compare it with angiographic and scintigraphic methods. A total of 27 patients with mitral regurgitation were evaluated by echocardiography and either cardiac catheterization or scintigraphy. With two-dimensional echocardiography, diastolic and systolic volumes were measured to derive the left ventricular stroke volume (LVSV). The forward stroke volume (FSV) was obtained from the product of M mode-derived aortic valve area and ascending aortic flow velocity integral assessed by continuous-wave Doppler. Regurgitant fraction was calculated as follows: (LVSV - FSV)/LVSV. Comparisons showed that regurgitant fraction calculated by Doppler echocardiography correlated with regurgitant fraction determined by both cardiac catheterization (r = .82) and by scintigraphy (r = .89). There was, however, an important interobserver variability within each method: 10%, 13%, and 11% for Doppler echocardiography, angiography, and scintigraphy, respectively. In conclusion, Doppler echocardiography can be used to quantitate mitral regurgitation. Serial noninvasive determinations of regurgitant fraction may be useful in the evaluation of therapy and in the follow-up of patients with mitral insufficiency.

Adult↗

Myocardial dysfunction in septic shock.

Myocardial depression is a major but poorly understood component of septic shock. This study investigates the morphologic and biochemical abnormalities associated with septic shock. Myocardial cells are incubated in normal and septic plasma in a nutrient-, oxygen-, pH-, electrolyte-, and temperature-controlled environment. Cells and media are tested for basal- and epinephrine-stimulated cyclic adenosine monophosphate (cAMP), lactic dehydrogenase (LDH), and creatine kinase. Electron microscopic studies are done at the end of incubation. Septic LDH and creatine kinase levels in the media are increased substantially, and septic cAMP levels are reduced significantly. Septic cells beat irregularly and arrest along with exhibiting abnormal electron microscopic structure. Septic myocardial dysfunction occurs independently of previously postulated causes that are controlled for in this experiment and therefore may be due to endogenously produced or accumulated toxic factor(s).

Animals↗

Interaction of "supplementary" scintigraphic indicators of ischemia and stress electrocardiography in the diagnosis of multivessel coronary disease.

Lung uptake, ventricular cavitary dilation and basal myocardial uptake represent abnormalities that have been associated with myocardial ischemia on stress thallium-201 images, but that are supplementary to the conventional assessment of perfusion distribution. These "supplementary" indicators of ischemia were related to the coronary distribution of perfusion abnormalities, the results of electrocardiographic stress testing and to the findings on coronary angiography in 73 patients. Forty patients had multivessel coronary disease; 19 of these had three vessel disease. Perfusion abnormalities were seen in 39 of these 40 patients but were indicative of multivessel coronary disease in only 28 and of three vessel disease in only 6. However, supplementary indicators were present in 33 of 40 patients with multivessel disease and in 15 of 19 with three vessel disease. Furthermore, they were seen in 16 of 22 patients with multivessel disease in whom conventional perfusion abnormalities underestimated the extent of disease, but in only 4 of 12 patients in whom the extent of disease was overestimated. The presence of either perfusion abnormalities in a multivessel distribution or supplementary indicators identified 38 (95%) of 40 patients with multivessel disease. A markedly positive electrocardiographic treadmill test was a less sensitive indicator of multivessel disease, appearing in only 15 of 40 patients. However, it was present in only 4 of 33 patients without multivessel coronary disease and was more specific for that diagnosis than were supplementary scintigraphic indicators (88 versus 67%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The etiology and implications of dense cavitary "photopenia" on myocardial perfusion scintigraphy.

Dense cavitary "photopenia" was observed on 21 of 200 consecutive stress perfusion scintigrams. A prominent finding in many cases, it sometimes occupied only a portion of the region overlying the ventricular cavity, was often seen in some projections and not others, and was frequently adjacent to myocardial perfusion defects. To distinguish an etiology among reduced cavitary radioactivity, relatively increased background radioactivity, or reduced radioactivity in overlying myocardium, quantitative analysis of cavitary, lung and myocardial radioactivity was performed in patients with dense cavitary "photopenia," with and without lung uptake, and compared with results from studies showing increased lung uptake without cavitary photopenia and with normal studies. The results showed that dense cavitary photopenia was related to reduced radioactivity in overlying myocardium. Correlative imaging studies performed with echocardiography and contrast ventriculography confirmed this relationship to myocardial scar in 15 of 21 patients in whom associated akinesis or dyskinesis was seen. Hence, dense cavitary photopenia on stress perfusion scintigraphy is due to a dense myocardial perfusion abnormality, and is often indicative of related scar and an associated severe contraction abnormality.

Adult↗

The effects of coronary angioplasty and reperfusion on distribution of myocardial flow.

To assess the effects of angioplasty (PTCA) and intracoronary streptokinase (ICSK) on relative myocardial perfusion, we administered 99mTc-macroaggregated albumin (MAA) to the uninvolved coronary artery before successful PTCA in 33 patients and before successful infusion of ICSK in eight patients and of 111In-MAA into the same vessel after the intervention. In 10 patients who underwent PTCA, MAA was injected into the involved, instrumented coronary artery. Computer-processed images were acquired in registry and compared. Similar scintigraphic studies were performed in six control patients and in 11 in whom planned interventions were not performed or were unsuccessful. Distribution of MAA was also compared with angiographic results and with the distribution of 201Tl on images obtained in patients at rest or on redistribution images obtained before and soon after intervention in 22 patients. In control patients and those studied after aborted or unsuccessful intervention, scintigraphic results showed excellent correlation with the angiographic anatomy and were without serial change. When MAA was injected into the uninvolved vessel, the scintigram revealed evidence of collateral perfusion with retraction of the perfusion zone from that of the involved coronary in 19 of 33 patients undergoing PTCA and in three of eight of those receiving ICSK. When MAA was injected into the involved artery, a relative increase in perfusion was seen in eight of 10 patients after PTCA. Although 30 patients demonstrated scintigraphic evidence of collateral vessels, only 10 patients had angiographic evidence of collateral circulation before intervention. The distribution of 201Tl demonstrated little change in its global pattern and regions previously supplied by collaterals were generally well perfused after intervention. Coronary collateral perfusion may be inapparent angiographically and regress rapidly after angioplasty or reperfusion. Native perfusion is generally and quickly restored after successful PTCA or ICSK infusion, which obviates the need for collaterals. After intervention, the distribution of total perfusion may not change, but its regional source may demonstrate beneficial alterations, shifting from collateral to native circulation.

Angioplasty, Balloon↗