Yoshihiko Adachi

Assessment of ampulla (Takotsubo) cardiomyopathy with coronary angiography, two-dimensional echocardiography and99mTc-tetrofosmin myocardial single photon emission computed tomography

We studied the causative mechanism of ampulla (Takotsubo) cardiomyopathy.Methods: We examined 7 patients with ampulla cardiomyopathy by means of coronary angiography, two-dimensional echocardiography and99mTc-tetrofosmin myocardial SPECT at the time of emergency admission (acute phase), at 3 to 5 days after the attack (subacute phase) and at 1 month after the attack (chronic phase). The left ventricle was divided into 9 regions on two-dimensional echocardiograms and99mTc-tetrofosmin myocardial SPECT images, then the degree of abnormalities in each region was scored in four grades from normal (0) to severely abnormal (3). We injected nicorandil into the coronary arteries and determined the elevation in the ST segment before and after administration.Results: Coronary angiography did not show stenotic lesions in any patient. The acute, subacute and chronic phase myocardial perfusion scores on99mTc-tetrofosmin myocardial SPECT were 11.2±3.4, 2.7±2.3 and 0.4±0.5, respectively, and wall motion scores on echocardiograms were 13.0±3.6, 4.4±2.2 and 0.6±0.6, respectively, indicating improvement in all scores during the subacute phase (p<0.01). The elevation in the ST segment (mm) on the electrocardiogram was improved from 8.3±2.7 to 4.9±1.9 after the administration of nicorandil (p<0.05).Conclusion: These findings indicated that coronary microvascular spasm in one causative mechanism of ampulla cardiomyopathy.

Assessment of transient left ventricular dilatation on rest and exercise on Tc-99m tetrofosmin myocardial SPECT.

In myocardial perfusion imaging, multiple-vessel involvement of coronary artery disease (CAD) sometimes makes diagnosis difficult. Transient left ventricular (LV) dilatation on Tl-201 myocardial SPECT is a useful finding that enables the clinician to identify patients with multiple-vessel disease. The aim of this study was to confirm the utility of measuring transient LV dilatation for the detection of multiple-vessel CAD in exercise Tc-99m tetrofosmin myocardial SPECT. The participants were 55 CAD patients and 20 controls who underwent Tc-99m tetrofosmin myocardial SPECT exercise and resting imaging. During exercise, 370 MBq (10 mCi) Tc-99m tetrofosmin was injected. Exercise images were obtained 30 minutes after injection. At 210 minutes after injection, 740 MBq (20 mCi) Tc-99m tetrofosmin was administered intravenously. The rest SPECT images were acquired 30 minutes later. Thirty-six radii at every 10 degrees were generated from the center of short-axis images. An area surrounded by 36 maximal points of the myocardial Tc-99m tetrofosmin counts on each radius was calculated for exercise and rest images. The area surrounded by the 36 maximal points in the same slice of the exercise and rest images was assigned the variables A (Ex) and A(R), respectively. The transient dilatation index (TDI) of the left ventricle was calculated using the formula mean A (Ex)/A(R) in the apical, middle, and basal myocardial short-axis images. In the controls, the TDI was 0.970 ± 0.021. In patients with CAD, the TDIs of one-vessel disease, two-vessel disease, and three-vessel disease were 1.034 ± 0.032, 1.093 ± 0.046, and 1.131 ± 0.076, respectively. The TDIs were significantly greater in patients who had more occluded coronary arteries (P < 0.01). If the mean + 2SD of the TDI (1.012) in controls were assumed to be the normal upper limit, the sensitivity, specificity, and accuracy of this method in detecting two-vessel or three-vessel disease would be 91.4%, 76.9%, and 84%, respectively. The TDI is a useful index for evaluating subendocardial ischemia noninvasively and detecting multiple-vessel disease clinically.

Uncommon and dynamic changes detected by123I-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid myocardial single photon emission computed tomography in a stunned myocardium induced by coronary microvascular spasm

A 55-yr-old man underwent surgery. Soon after the procedure was finished, the patient complained of chest pain, and the electrocardiogram showed increase in the ST-segment in some leads. Emergency angiography showed normal coronary arteries, but there was asynergy in the left ventricle, and delayed filling of contrast medium was observed in the LCA. An intracoronary infusion of isosorbide dinitrate did not improve the delayed filling of contrast medium or ST segment increase in the electrocardiogram. Soon after nicorandil was injected into the LCA, the patients symptoms, electrocardiogram, and delayed filling of contrast medium dramatically improved. On the second day, initial imaging by123I-BMIPP myocardial SPECT showed a moderate increase in tracer uptake in the apico-anteroseptal region and a moderate decrease in tracer uptake in the lateral region, in which the first left ventriculography showed akinesis, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of123I-BMIPP in the anteroseptal and lateral regions. On the sixth day, initial imaging by123I-BMIPP myocardial SPECT showed a moderate decrease in tracer uptake in the apical and lateral regions and a mild decrease in tracer uptake in the anteroseptal region, and delayed imaging revealed a moderate increase in tracer uptake in the apical region and a high washout of123I-BMIPP in the anteroseptal and lateral regions. By the 30th day,123I-BMIPP myocardial SPECT had normalized. We consider that these dynamic changes in123I-BMIPP myocardial SPECT imaging may reflect metabolic changes in fatty acids in the ischemic state, the size of the triacylglycerol pool, and the degree of turnover in the triacylglycerol pool.

Long-term follow-up of myocardial perfusion and metabolic images in a patient with hypertrophic cardiomyopathy.

A 54-year-old woman was hospitalized in 1989 because of palpitations. She had a family history of hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy was diagnosed by two-dimensional echocardiography, cardiac catheterization, and myocardial biopsy. A coronary arteriogram disclosed normal coronary arteries. She had received diltiazem and meliletine for 9 years. Her functional class, by the New York Heart Association classification, had worsened from II to III since 1995. Two-dimensional echocardiography showed a thrombus in the left ventricle in 1996, and warfarin and captopril were prescribed. Follow-up images showed that 1-123 β-methyl-p-iodophenyl-pentadecanoic acid uptake preceded that of TI-201.

Surgical Removal of Intra-Aortic Balloon Catheter With Fractured Nitinol Central Lumen

A 73-year-old woman suffering from septic shock was given circulatory assistance by intra-aortic balloon pumping (IABP). Eleven hours later, pumping stopped abruptly and blood reflux was observed in the intra-aortic balloon catheter (IABC). We removed it and inserted another IABC; 3.5 h later, pumping stopped again and blood reflux was seen. Removal of the IABC was attempted, as the systolic aortic pressure remained above 100 mmHg, but there was resistance during the removal and as a result 7.5cm of the catheter from the tip remained inside the vessel. Fluoroscopy indicated that the metal tube that formed the central lumen in the balloon was fractured, and that its edge had perforated the femoral artery. The balloon was then removed surgically. Fracture of the metal tube and balloon perforation were confirmed in both the damaged IABCs. Postoperative computed tomography and magnetic resonance imaging indicated a highly severe posterior-anterior bend in the patients aorta. A vessel model similar to the aorta in this case was made and a reproducibility test was conducted; the central lumen fractured within 3 h and under a microscope the profile of the fractured test lumen was similar to the one in the clinical case. These findings suggest that placing a pumping IABC in a bending aorta causes fracture of the central lumen from fatigue failure because the central lumen is under excessive stress.

Increasing myocardial123I-BMIPP uptake in non-ischemic area in a patient with acute myocardial ischemia

The subject was a 65-year-old woman with chest pain. An electrocardiogram revealed T-wave-inversion in leads III, aVF, V1–V5.99mTc-tetrofosmin myocardial SPECT showed mildly reduced uptake in the anteroseptal wall and the apex. These findings suggested acute myocardial ischemia. Coronary angiography did not show any stenotic lesions, but diffuse coronary ectasia was noted in three vessels. Coronary flow velocity was remarkably reduced on coronary angiography. Epicardial coronary spasm was not provoked by ergonovine loading test. Left ventriculography showed diffuse hypokinesis.123I-BMIPP myocardial SPECT showed mildly reduced uptake in the anteroseptal wall and the apex on the early images. But 4-hour delayed images showed an increase of 8% in myocardial123I-BMIPP uptake. We treated this patient with ticlopidine and nicorandil. After drug therapy her symptoms and left ventriculography improved.123I-BMIPP myocardial SPECT findings on the early images improved, whereas delayed images showed a decrease of 28% in myocardial123I-BMIPP uptake after two weeks and 36% after four weeks. These dynamic changes in123I-BMIPP findings might be a reflection of myocardial fatty acid metabolism in patients with acute myocardial ischemia. Delayed123I-BMIPP myocardial SPECT images are useful for the assessment of fatty acid metabolism.

A patient with type I CD36 deficiency whose myocardium accumulated 123I-BMIPP after 4 years

A 73-year-old man with aortic regurgitation was examined by123I-α-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) myocardial single photon emission computed tomography (SPECT) in 1995. Myocardial accumulation was not evident on either the early or the delayed image obtained 15 minutes and 3 hours, respectively, after injecting123I-BMIPP. Flow cytometric analysis of CD36 expression in monocytes and platelets identified a type I CD36 deficiency. The patient was hospitalized for severe heart failure in 1999. Upon admission, the cardiothoracic ratio on chest X-rays was 73%, and the left ventricular end-diastolic diameter on echocardiograms was enlarged to 77 mm. On the second day, we performed123I-BMIPP myocardial SPECT. Myocardial accumulation was evident in the delayed, but not in the early image. We repeated123I-BMIPP myocardial SPECT on the 10th day after admission. Myocardial accumulation was evident on both early and delayed images.99mTc-tetrofosmin myocardial SPECT was immediately performed after123I-BMIPP myocardial SPECT to distinguish myocardial from pooling images in the left ventricle, but, because the images from both99mTc-tetrofosmin and123I-BMIPP myocardial SPECT were idential, we considered that the123I-BMIPP myocardial SPECT images reflected the actual myocardial condition.The CD36 molecule transports long-chain fatty acid (LCFA) on the myocardial membrane, but123I-BMIPP scintigraphy does not show any myocardial accumulation in patients with type I CD36 deficiency, indicating that myocardial LCFA uptake occurs through CD36 on the human myocardial membrane. Even though our patient had type I CD36 deficiency, BMIPP was uptaken by the myocardium during heart failure, suggesting a variant pathway on the human myocardial membrane for LCFA uptake.