Shuji Katoh

Assessment of Takotsubo (ampulla) cardiomyopathy using 99mTc-tetrofosmin myocardial SPECT--comparison with acute coronary syndrome.

We assessedTakotsubo (ampulla) cardiomyopathy compared with acute coronary syndrome (ACS) using two-dimensional echocardiography and99mTc-tetrofosmin myocardial SPECT.Methods: We examined 10 patients withTakotsubo cardiomyopathy and 16 with ACS at the time of emergency admission (acute phase), at three to nine days after the attack (subacute phase) and at one month after the attack (chronic phase). The left ventricle was divided into nine regions on echocardiograms and SPECT images, and the degree of abnormalities in each region was scored in five grades from normal (0) to severely abnormal (4).Results: Coronary angiography revealed total or subtotal occlusion in patients with ACS but no stenotic legions in those withTakotsubo cardiomyopathy. The amount of ST segment elevation (mm) was 7.9±3.4 in patients withTakotsubo cardiomyopathy and 7.3±3.7 in those with ACS (N.S.). Abnormal wall motion scores on echocardiograms were 13.8±4.4, 4.4±3.8 and 1.8±2.3 during the acute, subacute and chronic phases in patients withTakotsubo cardiomyopathy and 13.9±4.0, 11.7±3.7, 7.6±4.2, respectively in patients with ACS. The value of MB fraction of creatine phosphokinase (IU/l) was 34±23 in patients withTakotsubo cardiomyopathy and 326±98 in those with ACS (p<0.001). Abnormal myocardial perfusion scores on99mTc-tetrofosmin myocardial SPECT were 11.4±3.2, 3.2±3.3 and 0.7±1.1 during the acute, subacute and chronic phases respectively, in patients withTakotsubo cardiomyopathy, and 15.8±4.1, 13.5±4.4, 8.2±4.4, respectively, in those with ACS. The numbers of myocardial segments that did not uptake99mTc-tetrofosmin during the acute phase were 0.5±0.8 and 3.6±2.8 in patients withTakotsubo cardiomyopathy and ACS, respectively.Conclusion: Impaired coronary microcirculation might be a causative mechanism ofTakotsubo cardiomyopathy.

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.

Sudden Death Due to Rupture of Coronary Aneurysm in a 26-Year-Old Man

A 26-year-old man, previously in good health, was transferred to the emergency unit of our hospital on July 19, 1995; however, he was dead on arrival. He was an employee of a machine industry with no history of chest pain or palpitation, and at company checkups, no abnormalities were pointed out except for marked left hilar calcification on chest radiograph in June 1991 (Fig 1⇓); moreover, when he was 1 year old, he suffered from an acute self-limited febrile illness with diffuse erythematous macular rash followed by membranous desquamation of the fingertips and notable conjunctival infection resembling Stevens-Johnson syndrome or mucocutaneous lymph node syndrome that occurred 2 years after the first description of Kawasaki …

Investigation of the relationship between regression of hypertensive cardiac hypertrophy and improvement of cardiac sympathetic nervous dysfunction using iodine-123 metaiodobenzylguanidine myocardial imaging

Although many theories exist on the subject, the mechanisms responsible for a reduction of hypertensive cardiac hypertrophy in response to antihypertensive therapy are still unclear. In order to investigate the relationship between regression of hypertensive cardiac hypertrophy and cardiac nervous function, we studied ten patients with untreated essential hypertension (six men and four women, 62±12 years old). Both echocardiography and iodine-123 metaiodobenzylguanidine (MIBG) myocardial imaging were performed before and after antihypertensive therapy. Left ventricular mass (LVM) was significantly reduced in conjunction with the reduction of blood pressure following treatment. MIBG myocardial images showed that the heart-to-mediastinum activity ratio (H/M) was significantly increased while the washout ratio was significantly decreased. Patients were divided into two groups according to the ratio of the LVM values before and after therapy (LVM ratio). Patients with an LVM ratio of less than 0.75 were classified as group A and those with values higher than 0.75 as group B. Neither the change in blood pressure nor the length of treatment was significantly different between these two groups. On the other hand, both the increase in H/M and the decrease in the washout ratio were significantly greater in group A than in group B. These results indicate that an improvement in cardiac sympathetic nervous function may be related to the regression of hypertensive cardiac hypertrophy. Increasing the subject base in these studies and a more precise analysis of the relevance of the data obtained from MIBG myocadial images are recommended to clarify how changes in cardiac sympathetic nervous function relate to the regression of hypertensive cardiac hypertrophy.

Dynamic changes in cardiac fatty acid metabolism in the stunned human myocardium

BackgroundThe chronological changes or mechanisms in cardiac fatty acid metabolism under clinical conditions of hypoxia and ischemia have not been fully elucidated.123I-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) can be used with single photon emission computed tomography (SPECT) to evaluate myocardial fatty acid metabolism. We investigated chronological changes in energy metabolism in the stunned human myocardium by means of123I-BMIPP myocardial SPECT.Methods and ResultsWe conducted123I-BMIPP myocardial SPECT in 10 patients with stunned myocardium during the acute, subacute and chronic phases after onset. The left ventricle was divided into 9 regions on SPECT, and the degree of abnormalities in each region was scored in four grades from normal (0) to defect (4). We also examined wash-out rates on BMIPP images. The scores on early BMIPP images in the acute, subacute and chronic phases were 5.6±1.8, 13.4±3.5 and 2.5±1.1, respectively, and the score was highest in the subacute phase (p<0.001). Similarly, scores on the late images were 2.3±1.7, 18.3±4.5 and 4.7±2.6, respectively, and highest in the subacute phase (p<0.001). The wash-out rates (normal: 18.2±2.1%) in the acute, subacute and chronic phases were 12.1±4.8%, 44.9±10.0% and 23.1±4.6%, respectively, with the value being lowest during the acute phase (p<0.05), and highest during the subacute phase (p<0.001).ConclusionThese results suggested that fatty acid metabolism in the stunned human myocardium changes dynamically over time.

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.

Case report : left ventricular apical hypertrophy in progressive limb-girdle muscular dystrophy

Cardiac involvement is uncommon in patients with limb-girdle muscular dystrophy. This report describes a patient in whom concentric hypertrophy localized to the apical left ventricle was revealed during a long clinical course of skeletal muscular dystrophy, with evolving electrocardiographic changes also compatible with apical hypertrophic cardiomyopathy. Endomyocardial biopsy revealed similar histologic changes in the skeletal muscle biopsy specimen, characterized by muscle fiber atrophy and hypertrophy with a mild degree of interstitial fibrosis. The pathogenesis of cardiac hypertrophy in this case is unclear. However, the pathologic findings suggest that the myocardium may be involved in the same dystrophic process as the skeletal muscles.

Lanthanum carbonate for hyperphosphatemia in patients on peritoneal dialysis.

♦ Background: The efficacy of the phosphate binder lanthanum carbonate has been demonstrated for hemodialysis patients, but no studies have focused on patients undergoing continuous ambulatory peritoneal dialysis (CAPD). We evaluated whether lanthanum carbonate could control phosphate levels in patients on CAPD. ♦ Methods: In this 48-week open-label prospective study, 28 patients on CAPD with a phosphate level of 6 mg/dL or greater were given lanthanum carbonate titrated from 750 mg to 2250 mg daily to achieve a target serum phosphate level of less than 6 mg/dL. The primary efficacy endpoint was reduction of serum phosphate to less than 6 mg/dL. Serum levels of calcium and parathyroid hormone were also evaluated, as were the Ca×P product and adverse effects. ♦ Results: From week 4 to the end of the study at week 48, we observed a significant reduction of serum phosphate to 5.25 ± 0.97 mg/dL from 6.88 ± 1.06 mg/dL at study start (p < 0.01). At the end of the study, 78.6% of participants had achieved the target of less than 6 mg/dL. Because no change of serum calcium occurred, the Ca×P product declined significantly during the study. Intact parathyroid hormone declined gradually over the study period, but the change had not reached significance at the end of the study (p = 0.11). The mean final dose of lanthanum carbonate was 946 mg daily. The only adverse effect reported was mild nausea in 1 patient. ♦ Conclusions: Lanthanum carbonate is an effective phosphate binder that can control serum phosphate and Ca×P product in CAPD patients with hyperphosphatemia. Lanthanum carbonate was well tolerated in our population.

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.

Non-machinery-based system for cell-free, concentrated autogenous ascitic fluid reinfusion.

A non-machinery-based system for the reinfusion of ascitic fluid was developed and assessed. In fundamental studies utilizing bovine serum, this procedure proved economical, quick and useful. The most suitable filter was PS-R (#405-2). Bovine serum with a protein concentration below 3.0 g/dl was treated using this system. Samples containing blood (prepared to 0.5% hematocrit) were also treated, but the treatment time required was double that of serum with the same protein concentration. In both cases the protein recovery ratios were about 90%. We conducted clinical studies on 62 occasions (machinery-based system; 31 times, non-machinery-based system; 31 times) on 19 cases of ascites refractory to treatment with various drugs including diuretics. Clarification of the differences between the non-machinery and the machinery-based system, indicated the former to be superior. This new procedure is easier because of its use of no machinery, and the high protein recovery ratio proved its usefulness.