Technetium-99m Stannous Pyrophosphate Research Articles

Positive Technetium-99m Stannous Pyrophosphate Myocardial Imaging in Three Patients with Left Ventricular Thrombus

Positive Technetium-99m Stannous Pyrophosphate Myocardial Imaging in Three Patients with Left Ventricular Thrombus

Usefulness of early positive technetium-99m stannous pyrophosphate scan in predicting reperfusion after thrombolytic therapy for acute myocardial infarction

To test the hypothesis that scans with technetium-99m pyrophosphate (Tc-99m-PPi) are positive when performed early after successful thrombolytic therapy for acute myocardial infarction (AMI), 16 consecutive patients with AMI who received thrombolytic therapy within 5 hours after the onset of chest pain were studied. Patients were included if chest pain lasted for >30 minutes, was unresponsive to sublingual nitroglycerin and was associated with at least 0.2 mV ST-segment elevation in at least 2 contiguous electrocardiographic leads. All patients received 1.5 million IU of streptokinase intravenously, a mean of 195 ± 99 minutes after onset of chest pain. Tc-99m-PPi scans and coronary cineanglograms were recorded 491 ± 156 minutes and 518 ± 202 minutes, respectively, after the onset of symptoms. Effective reperfusion was present in 10 patients, 6 of whom had positive Tc-99m-PPi scans (sensitivity of 60% to detect reperfusion). Of the 6 patients without effective reperfusion, 3 had positive Tc-99m-PPi scans (specificity of 50%, p >0.05). Analysis of the data using various definitions of effective reperfusion or artery patency yielded similar results. Thus, our findings indicate that early AMI scanning with Tc-99m-PPi does not accurately detect the presence or absence of reperfusion in patients with AMI after treatment with intravenous streptokinase. At this time, coronary cineangiography is the only reliable method to detect reperfusion promptly after thrombolytic therapy.

Value of indium-111 monoclonal antimyosin antibody for imaging in acute myocardial infarction

In most patients with chest pain, clinical history and observed electrocardiographic and enzymatic changes are sufficient to prove or rule out an acute myocardial infarction (AMI). However, in some patients these methods fail to rule out or do not allow to localize the site of an AMI. In patients admitted several days after the acute attack of chest pain, enzyme levels may have returned to normal and the electrocardiogram may not differentiate old from recent infarction. In addition, the enzyme changes after coronary artery bypass grafting may be comparable to those seen during an AMI, but confirmation of the diagnosis and localization of the AMI on the electrocardiogram may be difficult. Localization of myocardial infarction may also be difficult in patients with a left bundle branch block or Wolff-Parkinson-White syndrome. Finally, although infarct size has been estimated by measuring enzyme levels, these values may be less reliable as a marker of infarct size after thrombolytic therapy. To overcome these problems nuclear imaging techniques have been used, particularly technetium-99m stannous pyrophosphate imaging. 1,2 However, technetium stannous pyrophosphate has disadvantages. Persistent blood pool activity and low-grade uptake in the region of the heart may be confused. In addition, uptake by overlying ribs and sternum may make interpretation of the technetium pyrophosphate scan difficult. Also, one must wait at least 24 hours, and preferably 48 to 72 hours, after the onset of chest pain. These problems may be resolved if single photon emission computed tomography and blood pool overlay techniques are used. 3 Since monoclonal antimyosin antibody labeled to indium-111 was available in our laboratory a study was undertaken to assess the value of this antibody to localize an AMI. To study the value of this technique patients were selected in whom electrocardiographic changes allowed localization of the AMI.

Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension.

This study examined the effect of exposures to hyperbaric oxygen on the development of the edema and necrosis of muscle that are associated with compartment syndromes that are complicated by hemorrhagic hypotension. A compartment syndrome (twenty millimeters of mercury for six hours) was induced by infusion of autologous plasma in the anterolateral compartment of the left hind limb of seven anesthetized dogs while the mean arterial blood pressure was maintained at sixty-five millimeters of mercury after 30 per cent loss of blood volume. These dogs were treated with hyperbaric oxygen (two atmospheres of pure oxygen) and were compared with six dogs that had an identical compartment syndrome and hypotensive condition but were not exposed to hyperbaric oxygen. Forty-eight hours later, edema was quantified by measuring the weights of the muscles (the pressurized muscle compared with the contralateral muscle), and necrosis of muscle was evaluated by measuring the uptake of technetium-99m stannous pyrophosphate. The ratio for edema was significantly (p = 0.01) greater in dogs that had not been exposed to hyperbaric oxygen (1.15 +/- 0.01) than in the dogs that had been treated with hyperbaric oxygen (1.01 +/- 0.03), and the ratio for necrosis of muscle was also significantly (p = 0.04) greater in dogs that had not had hyperbaric oxygen (1.96 +/- 0.41) than in those that had been treated with hyperbaric oxygen (1.05 +/- 0.11). Comparisons were also made with the muscles of four normal control dogs and separately with the muscles of six normotensive dogs that had an identical compartment syndrome and normal blood pressure and were not treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed use of hyperbaric oxygen for treatment of a model anterior compartment syndrome

This study examines the effect of delayed exposure to hyperbaric oxygen on muscle necrosis and edema development following compartment syndromes in the canine hindlimb. Compartment syndromes (100 mm Hg for 8 h) were generated in one anterolateral compartment of six anesthetized dogs. After a 2-h delay, three 1-h hyperbaric oxygen treatments (2 atm absolute pure oxygen) were given during the next 12 h. Two days later, technetium-99m stannous pyrophosphate (99mTc Sn-PYP) was injected intravenously; 3 h later, samples were obtained from the pressurized and contralateral control muscles, weighed for edema development, counted for 99mTC Sn-PYP uptake, and evaluated histologically. Hyperbaric oxygen treatments, even when delayed 2 h, reduced muscle necrosis and intramuscular edema to negligible levels (p less than 0.05) compared with untreated animals. In addition, muscle morphology remained essentially normal in all hyperbaric oxygen-treated animals. We conclude that even if hyperbaric oxygen treatments are delayed 2 h, edema and muscle necrosis are reduced significantly in a model compartment syndrome.

Early positive technetium-99m stannous pyrophosphate images as a marker of reperfusion after thrombolytic therapy for acute myocardial infarction

Fourteen patients with transmural acute myocardial infarction (AMI) were treated with intravenous streptokinase a mean of 4 ± 1 hours after chest pain and underwent technetium-99m stannous pyrophosphate (Tc-99m-PPi) imaging 7 ± 2 hours after the onset of chest pain. The early Tc-99m-PPi images were obtained to test the hypothesis that an early, strongly abnormal Tc-99m-PPi image suggests reperfusion. Eleven of 14 patients had early peaking (within 16 hours) serum creatine kinase isoenzyme levels (CK-B) at a mean of 11 ± 3 hours. Ten of 14 patients had 3+ or 4+ acute Tc-99m-PPi images. Eight of 11 patients had patent infarct-related vessels at cardiac catheterization 15 days after AMI. One patient who had both an early positive Tc-99m-PPi image and CK-B peak level had an occluded infarct-related artery at catheterization. Acute left ventricular (LV) ejection fraction (EF) by radionuclide ventriculography was compared with LVEF on day 15, and improved from 0.37 ± 0.13 to 0.50 ± 0.16 (p = 0.004) in the 10 patients with strongly positive acute Tc-99m-PPi images. LVEF also improved from 0.37 ± 0.12 to 0.49 ± 0.15 (p = 0.003) in the 11 patients with early peaking serum CK-B values. Three patients without evidence of reperfusion failed to improve the LVEF from the initial value to the one obtained at hospital discharge. Six control patients had acute Tc-99m-PPi images 10 ± 2 hours after chest pain; none had strongly positive acute Tc-99m-PPi images, and the mean time to peak CK-B was 19 ± 5 hours. Strongly positive early Tc-99m-PPi images may be as reliable as early peaking CK-B in predicting successful reperfusion in patients receiving intravenous streptokinase therapy for AMI.

Electrocardiographic, enzymatic and scintigraphic criteria of acute myocardial infarction as determined from study of 726 patients (a MILIS study)

Methods for detecting acute. myocardial infarction (AMI) were compared in a prospective study of 726 patients with pain presumed to be caused by ischemia that lasted 30 minutes or longer and was associated with electrocardiographic changes (ST-segment deviation ≥0.1 mV and/or new Q waves or left bundle branch block). Using MB-CK values of more than 12 IU/liter as the standard criterion for detection of AMI, 639 patients (88%) were judged to have AMI. Total plasma CK values, technetium-99m stannous pyrophosphate images 48 to 72 hours after admission, and serial 12-lead electrocardiograms over 10 days were analyzed by investigators blinded to other clinical and laboratory data. For detection of AMI, total CK, electrocardiograms (ECGs) and pyrophosphate imaging were all highly accurate and sensitive (total CK accuracy 97%, ECG 92%, pyrophosphate 88%; total CK sensitivity 98%, ECG 96% and pyrophosphate 91%). However, both pyrophosphate and ECG were less specific than total CK (p <0.01) (total CK specificity 89%, pyrophosphate 64% and ECG 59%). The sensitivity (p <0.05) and accuracy (p <0.01) of total CK and pyrophosphate for those patients with Q-wave development were slightly greater than for those in whom Q waves did not evolve. The ECG was less accurate (p < 0.02) and pyrophosphate was less specific (p <0.04) in patients with prior MI compared with those with initial infarction. Pyrophosphate failed to detect larger infarcts than either the ECG or total CK (both p <0.01). However, combined pyrophosphate and electrocardiographic criteria were more accurate than pyrophosphate (p <0.01) or the ECG alone (p <0.03), and pyrophosphate was helpful in identifying infarcts considered “indeterminate” on the ECG. Although each method has certain limitations, individual and combined use of these diagnostic criteria represent powerful means for detecting AMI.

An Uncommon Case of Subendocardial Infarction Studied by Technetium-99m Stannous Pyrophosphate Myocardial Scintigraphy

An Uncommon Case of Subendocardial Infarction Studied by Technetium-99m Stannous Pyrophosphate Myocardial Scintigraphy

The functional implications of scintigraphic measures of myocardial ischemia and infarction

To compare serial functional and perfusion scintigraphic changes after myocardial infarction, we performed left ventricular (LV) cineanglograms and thallium (Tl)-201 myocardial perfusion scintigrams before and 1 hour, 2 days, 9 days, and 1 month after closed chest coronary occlusion in 14 dogs as survival permitted. Survivors were studied with technetium-99m (stannous) pyrophosphate (TcPYP) scintigrams at 48 hours, and at postmortem examination infarction was documented and measured after nitroblue tetrazolium (NBT) staining. The TcPYP image was abnormal in 10 dogs, each of which had infarcts on NBT staining measuring 3 to 23 gm. In all 14 dogs, perfusion scintigrams became abnormal and LV ejection fraction (EF) fell when measured within 48 hours of occlusion. In the nine late survivors studied over 1 week after the event, perfusion scintigrams and EF improved in those which developed infarcts and normalized in those without infarction. The decrement in LVEF after coronary occlusion generally showed serial improvement and correlated with the size of the defect in the accompanying Tl-201 scintigram ( r = 0.74). Tl-201 defect size seen in late studies correlated well with NBT infarct size ( r = 0.89) and TcPYP image infarct size ( r = 0.82), as it did with the decrement in LVEF noted in late studies ( r = 0.86). The results suggest that early perfusion scintigrams together with TcPYP images may be useful for estimating the amount of reversible dysfunction after coronary occlusion.

Validation of technetium-99m stannous pyrophosphate myocardial scintigraphy for diagnosing acute myocardial infarction more than 48 hours old when serum creatine kinase-mb has returned to normal

Determination of lactic dehydrogenase (LDH) isoenzymes is the current method of choice for diagnosing acute myocardial infarction (AMI) > 48 hours old. However, other causes of enzyme elevation make the availability of an alternate method of diagnosis worthwhile. Accordingly, serial technetium-99m pyrophosphate scintigrams were obtained in 61 patients with transmural AMI and in 46 patients with subendocardial AMI. Imaging was performed in all 107 patients at the time creatine kinase isoenzyme (CK-MB) was present 37 ± 18 hours (range 12 to 72) after the onset of AMI, and at the time CK-MB was absent 106 ± 34 hours (range 48 to 168) after the onset of AMI. At the time CK-MB was absent, the sensitivity using either a regional or a diffuse positive scintigram was 95% (58 of 61 patients) for transmural AMI and 65% (30 of 46 patients) for subendocardial AMI. The sensitivity using a regional positive scintigram was 82% (50 of 61 patients) for transmural AMI and 37% (17 of 46 patients) for subendocardial AMI. The sensitivity using a high-grade regional positive scintigram was 36% (22 of 61 patients) for transmural AMI and 11% (5 of 46 patients) for subendocardial AMI. The specificity was 70% (143 of 204 patients) for either a regional or a diffuse abnormality, 92% (187 of 204 patients) for a regional abnormality, and 100% (204 of 204 patients) for a high-grade regional abnormality. Thus, pyrophosphate scintigraphy is useful in confirming the diagnosis of AMI, particularly transmural, > 48 hours old and when CK-MB has returned to normal. A positive scintigram with a high-grade regional abnormality is specific for a recent AMI and may be contributory in establishing the diagnoses when LDH isoenzymes are inconclusive.

Detection of acute right ventricular infarction by right precordial electrocardiography

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V 4R to V 6R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 ± 14.3 (mean ± standard deviation) and 85.1 ± 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 ± 0.11) than in Group B (0.60 ± 0.12) (p < 0.01). Right ventricular total wall motion score was 63.8 ± 15.6 percent of normal in Group A versus 94.3 ± 8.5 percent in Group B (p < 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p < 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V 4R to V 6R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.

The high-risk angina patient: Identification by clinical features, hospital course, electrocardiography and technetium-99M stannous pyrophosphate scintigraphy : Olson HG, Lyons KP, Aronow WS, Stinson PJ, Kuperus J, Waters HJ. Circulation 64 No. 4, 1981

The high-risk angina patient: Identification by clinical features, hospital course, electrocardiography and technetium-99M stannous pyrophosphate scintigraphy : Olson HG, Lyons KP, Aronow WS, Stinson PJ, Kuperus J, Waters HJ. Circulation 64 No. 4, 1981

Increased incidence and clinical correlation of persistently abnormal technetium pyrophosphate myocardial scintigrams following acute myocardial infarction in patients with diabetes mellitus

“Persistently abnormal” technetium-99m stannous pyrophosphate myocardial scintigrams (PPi+) appear to be associated with a relatively poor prognosis after acute myocardial infarction (AMI). To assess the incidence and implications of PPi+, we performed a retrospective analysis in 29 patients with and 25 patients without diabetes mellitus who had abnormal myocardial scintigrams within 4 days of AMI and who had follow-up scintigrams at least 3 months after hospital discharge. There were no significant differences between patients with and without diabetes as regards age, incidence of transmural or nontransmural AMI, or degree of left ventricular dysfunction after AMI. Persistently abnormal PPi+ occurred more commonly in patients with diabetes than in nondiabetic patients (18 of 29, 62%, compared to 3 of 25, 12%; p < 0.001). Patients with chronic PPi+ had more frequent cardiac complications following hospital discharge ( p < 0.005) including death, recurrent AMI, unstable angina, and intractable congestive heart failure. Postmortem analysis in two patients with diabetes and chronic PPi+ revealed marked myocytolysis. Thus, patients with diabetes mellitus have an increased incidence of post-AMI “persistently abnormal” technetium (PPi+) scintigrams and relatively poor prognosis following myocardial infarction.

The high-risk angina patient. Identification by clinical features, hospital course, electrocardiography and technetium-99m stannous pyrophosphate scintigraphy.

We evaluated 193 consecutive unstable angina patients by clinical features, hospital course and electrocardiography. All patients were managed medically. Of the 193 patients, 150 (78%) had a technetium-99m pyrophosphate (Tc-PYP) myocardial scintigram after hospitalization. Of these, 49 (33%) had positive scintigrams. At a follow-up of 24.9 +/- 10.8 months after hospitalization, 16 of 49 patients (33%) with positive scintigrams died from cardiac causes, compared with six of 101 patients (6%) with negative scintigrams (p less than 0.001). Of 49 patients with positive scintigrams, 11 (22%) had had nonfatal myocardial infarction at follow-up, compared with seven of 101 patients (7%) with negative scintigrams (p less than 0.01). Age, duration of clinical coronary artery disease, continuing angina during hospitalization, ischemic ECG, cardiomegaly and a history of heart failure also correlated with cardiac death at follow-up. Ischemic ECG and a history of angina with a crescendo pattern also correlated with nonfatal infarction at follow-up. Patients with continuing angina, an ischemic ECG and a positive scintigram constituted a high-risk unstable angina subgroup with a survival rate of 58% at 6 months, 47% at 12 months and 42% at 24 and 36 months. We conclude that the assessment of clinical features, hospital course, ECG and Tc-PYP scintigraphy may be useful in identifying high-risk unstable angina patients.

Quantitation of skeletal-muscle necrosis in a model compartment syndrome.

Skeletal-muscle necrosis was evaluated in previously pressurized canine compartments using technetium-99m stannous pyrophosphate and classic histological criteria. Intracompartmental necrosis was quantitated in the anterolateral muscle compartment of each dog by uptake of 99mTc stannous pyrophosphate using the contralateral anterolateral compartment as an internal control. Representative specimens of muscle were sampled in experimental and control legs of each dog and were analyzed by qualitative histological techniques. Muscle necrosis was assessed in compartments forty-eight hours after pressurization to levels of ten to 120 millimeters of mercury for eight hours in thirty-seven dogs. In another dog, neither anterolateral compartment was pressurized so that both compartments acted as control muscle. The results in these experiments identify a threshold pressure level (thirty millimeters of mercury) and duration (eight hours) at which significant muscle necrosis occurs at normal blood pressure. Our findings imply that a quantitative relationship exists between incorporation of 99mTc stannous pyrophosphate and the level of intracompartmental pressure. This uptake technique, however, is not suitable for diagnosing compartment syndrome in patients with a threatened compartment syndrome. We suggest that intracompartmental pressure measurements by the wick-catheter technique, in conjunction with clinical findings, offer the best means for diagnosing compartment syndrome. Significant muscle necrosis associated with an impending compartment syndrome occurs at a threshold intracompartmental pressure of thirty millimeters of mercury after eight hours. Since time variables are often unknown in suspected compartment syndromes, fasciotomy is recommended when intracompartmental pressure exceeds thirty millimeters of mercury in a patient with normal blood pressure. The use of this threshold pressure level as an indication for fasciotomy requires a device for measuring intracompartmental pressure such as the wick catheter.

Noninvasive methods for detection of valve vegetations in infective endocarditis

To determine the optimal noninvasive method for the demonstration of endocarditic vegetations, 35 consecutive episodes of clinically diagnosed endocarditis in 33 patients were studied with M mode and two dimensional echocardiography, and with gallium-67 citrate and technetium-99m stannous pyrophosphate cardiac scanning. Clinical criteria for the diagnosis of endocarditis were: temperature higher than 38 ° C; sustained bacteremia with at least three positive blood cultures; no extracardiac focus of bacteremia; and known underlying heart disease, a new or changing murmur or a history of intravenous drug abuse with radiologic evidence of septic pulmonary emboli. M mode echocardiography detected 18 vegetations in 17 of the 35 episodes of endocarditis studied (49 percent positive); two dimensional echocardiography detected 30 vegetations in 28 of the 35 episodes studied (80 percent positive). In contrast, no vegetations were detected with technetium-99m stannous pyrophosphate scanning, and only two gallium-67 citrate scans were positive. The advantage of the two dimensional echocardiographic technique over all others tested was particularly notable for the identification of aortic and tricuspid valve vegetations.

Estimation of myocardial involvement in patients with acute myocardial infarction by two-dimensional echocardiography.

To determine whether real-time two-dimensional echocardiography (2-D echo) can estimate the extent of myocardial involvement in patients with acute myocardial infarction (MI), regional wall motion on serial short-axis 2-D echo recordings was analyzed and the summed scores were compared with estimates of infarct involvement by thallium-201 reperfusion (Tl) and technetium-99m stannous pyrophosphate (99mTc-PYP) scintigraphy. Thirty-two consecutive male patients admitted with their first MI were studied; 10 patients had anterior, 16 had inferior and six had subendocardial MIs. Two patients were technically unsuitable for 2-D echo studies. Twenty patients had Tl scintigrams and 29 had 99MTc-PYP scintigrams. Summed 2-D echo scores correlated closely with estimates of infarct involvement by Tl (r = 0.87) and with estimates of infarct size by 99mTc-PYP (r = 0.74). The location of MI by 2-D echo agreed with the electrocardiographic location in 26 of 29 patients; discrepancies occurred in one inferior and two subendocardial MIs. Predischarge 2-D echo failed to identify extension of transmural infarction. However, two patients whose subendocardial MIs progressed to transmural MIs were identified. This study shows that 2-D echo is a valid method for the early estimation of the extent of myocardial involvement in patients with acute MI, especially transmural MIs. In particular, 2-D echo correlates closely with Tl reperfusion scintigraphy because both detect areas of ischemia and infarction.

Skeletal muscle necrosis in pressurized compartments associated with hemorrhagic hypotension.

Skeletal muscle necrosis is quantified using technetium-99m stannous pyrophosphate (99mTc-PYP) in pressurized muscle compartments after severe blood loss. Six dogs (15 to 20 kg) were anesthetized by pentobarbital sodium (25 mg/kg IV) and hemorrhaged to a hypotensive state. Left hind-leg muscle compartments were pressurized to a level of 20 mm Hg for 6 hours by infusing autologous plasma. Intracompartmental pressure was continuously monitored by the wick catheter. The right leg served as a control. Forty-eight hours following pressurization, 5 mCi of 99mTc-PYP were injected IV, and 3 hours later each dog was sacrificed and pressurized and control muscles were resected simultaneously, weighed, and counted for 99mTc-PYP uptake. Significant uptake appeared in muscle compartments pressurized for 6 hours at 20 mm Hg, indicating that 20 mm Hg in a hypotensive state produces a degree of necrosis as great as that produced by 40 to 50 mm Hg in a normotensive state. We conclude that an acute compartment syndrome occurs in a hypotensive individual at an intramuscular pressure level considerably less than the threshold pressure level in an individual with normal blood pressure.

Diagnostic criteria for acute myocardial infarction in patients undergoing coronary artery bypass surgery.

Current techniques for diagnosing perioperative myocardial infarction were studied in 58 patients who underwent coronary bypass surgery. All patients had preoperative and postoperative ECGs and technetium-99m stannous pyrophosphate myocardial scintigrams; serum CK-MB was measured immediately after surgery and daily for 3 days. Postoperative bypass graft visualization and left ventriculography were performed before hospital discharge in every patient. Nine patients (16%) had new Q waves postoperatively. Five of these nine patients had positive pyrophosphate scintigrams, postive CK-MB and new wall motion abnormalities, and the remaining four had negative CK-MB, negative phyrophosphate scintigrams and no new wall motion abnormalities. Seven patients (12%) had newly positive postoperative pyrophosphate scintigrams, positive CK-MB and new wall motion abnormalities on postoperative ventriculography, but only four had new Q waves postoperatively. Eight patients (14%) had new wall motion abnormalities; seven had positive pyrophosphate scintigrams and all had positive CK-MB, but only five had new Q waves. Sixteen patients (28%) had positive CK-MB, including all patients with either positive pyrophosphate scintigrams or new wall motion abnormalities, Eight patients had positive CK-MB without other evidence of perioperative infarction. A newly positive postoperative pyrophosphate scintigram is more senstive and specific than the development of new postoperative Q waves for the diagnosis of hemodynamically significatn perioperative myocardial in farction. CK-MB is highly sensitive, but too nonspecific to be useful for the diagnosis of perioperative infarction.

Radioimmunoassay of serum creatine kinase B isoenzyme in the diagnosis of acute myocardial infarction: Correlation with technetium-99m stannous pyrophosphate myocardial scintigraphy

In 80 patients admitted to a coronary care unit within 24 hours of chest pain thought to be due to acute myocardial infarction, routine diagnostic tests (electrocardiograms, total serum creatine kinase) as well as 99mtechnetium stannous pyrophosphate, TcPYP myocardial scintigraphy and serial serum radioimmunoassay determinations of the B subunit of creatine kinase (CK-B), were performed. None of these patients had clinical evidence of acute cerebral injury. A definite decision regarding the presence of acute myocardial infarction could be made in 77 patients on the basis of the results of routine diagnostic tests. The calculated sensitivity, specificity and predictive value of an elevated serum CK-B level in the recognition of acute myocardial infarction were each 100 per cent. Serial TcPYP scintigraphy was 97 per cent sensitive and 70 per cent specific, and had a predictive value of 96 per cent for the recognition of acute myocardial infarction. Both serum CK-B analysis and TcPYP myocardial scintigraphy were helpful in the recognition of infarct extension, and serial studies with both techniques suggested the presence of asymptomatic extension of infarction in several patients. The predictive value of each of these techniques for the recognition of a myocardial infarct suggests that both may be of diagnostic assistance to the physician in clinical settings in which the history, electrocardiogram or total serum creatine kinase are for some reason not interpretable. These techniques may also prove complementary in furthering the ability to assess the extent of acute myocardial damage and the course of its progression.