Clinical characteristics of silent myocardial ischemia diagnosed with adenosine stress 99mTc-tetrofosmin myocardial scintigraphy in Japanese patients with acute cerebral infarction.

It is well known that silent myocardial ischemia (SMI) often complicates patients with cerebral infarction and that stroke patients often die of ischemic heart disease. Therefore, it is considered important to treat myocardial ischemia in stroke patients. This study investigated SMI complicating Japanese patients with fresh stroke, using (99m)Tc-tetrofosmin myocardial scintigraphy with pharmacologic stress testing to elucidate their clinical manifestations. This study included 41 patients (26 men, mean age 76.0 ± 10.7 years) with acute cerebral infarction and no history of coronary artery disease. All patients underwent (99m)Tc-tetrofosmin myocardial scintigraphy with intravenous administration of adenosine to diagnose SMI. Of the 41 patients, myocardial ischemia was confirmed in 17 patients (41.5%). Atherosclerotic etiology was the major cause of stroke in the ischemia(+) group and embolic origin was the major cause in the ischemia(-) group. Patients with myocardial ischemia had a higher incidence of diabetes mellitus (52.9 vs 20.8%; P = 0.0323) and more than two conventional cardiovascular risk factors (64.7 vs 25.0%; P = 0.0110) compared with the nonischemic patients. Infarction subtype of atherosclerotic origin was an independent positive predictor of asymptomatic myocardial ischemia in patients with stroke. These findings indicate that the prevalence of asymptomatic myocardial ischemia is relatively high, especially in patients with stroke of atherosclerotic origin. Therefore, it is beneficial for us to narrow the target population who are at the highest risk when screening for SMI in Japanese patients with acute cerebral infarction.

Effects of cardiologist experience on outcomes of patients with ST-elevated myocardial infarction treated with primary PCI in a local area in Japan.

Primary percutaneous coronary intervention (PCI) for ST-elevated myocardial infarction (STEMI) results in dramatically improved clinical outcomes when performed in a timely manner. Although guidelines for STEMI patients recommend PCI should be performed by experienced operators with acceptable PCI volume, cardiologists in a local area must perform primary PCI at their own hospitals. This study evaluated the effects of cardiologist experience on outcomes for STEMI patients in a local area in Japan.Between April 2007 and March 2010, 140 consecutive STEMI patients were admitted to our hospital and 121 of these patients received primary PCI. STEMI patients undergoing primary PCI were divided into two groups according to the operator's experience as a cardiologist. We retrospectively analyzed their clinical backgrounds, PCI findings, in-hospital outcomes, and drug administration at discharge.There were no significant differences in any clinical characteristics, angiographic findings, or PCI procedures between the two groups. Clinical outcomes of the two groups were similar, except for the length of hospital stay (21.1 ± 5.8 versus 15.5 ± 9.7; P = 0.0255). The frequency of administration of drugs such as ß-blockers (59.1% versus 34.0%; P = 0.0086), aldosterone blockade (10.4% versus 25.5%; P = 0.0334), and nicorandil (76.1% versus 25.5%; P = < 0.0001) was different between the two groups.The clinical outcomes of STEMI patients in this study were satisfactory and almost equivalent when compared according to the experience of the attending cardiologist. The present findings suggest the important clinical implication that younger cardiologists who have experienced PCI procedures to a certain extent can safely perform primary PCI and contribute to better prognoses of STEMI patients.

Clinical manifestations and effects of primary percutaneous coronary intervention for patients with delayed pre-hospital time in acute myocardial infarction.

BACKGROUND: Prolonged pre-hospital time for acute myocardial infarction (AMI) is associated with decreased indication for primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI in AMI patients with prolonged pre-hospital time has not been fully investigated in Japan. METHODS AND RESULTS: A total of 3010 consecutive AMI patients admitted to AMI-Kyoto Multi-Center Risk Study Group hospitals were retrospectively analyzed, and the clinical characteristics and in-hospital prognosis of these patients were reviewed. Patients with pre-hospital delay [elapsed time (ET)>12 h] had a lower frequency of Killip≥3 (9.3%) and less frequently received primary PCI (77.7%) compared with patients with ET≤12 h. In the ET>12 h group, older patients or patients with MI history tended to be complicated by heart failure. Primary PCI was performed for patients with ET>12 h, irrespective of the severity of heart failure [Killip 1 (78.7%) vs Killip≥2 (74.0%); p=0.3827]. On multivariate logistic regression analysis, age [odds ratio (OR) 1.053], MI history (OR 2.860), Killip≥2 (OR 10.235), and multi-vessels or left main coronary artery as culprit (OR 11.712) were significant independent positive predictors of in-hospital mortality for patients with ET>12 h. Practice of primary PCI was not a significant negative predictor for patients with ET>12 h (OR 0.812), but it was for patients with ET≤12 h (OR 0.425). CONCLUSIONS: These findings indicate that patients with ET>12 h have a less severe condition and less frequently receive primary PCI compared with patients with ET≤12 h. Although primary PCI is often performed for these patients irrespective of the severity of heart failure, no preferable effect of primary PCI on the in-hospital mortality is demonstrated. In contrary, practice of primary PCI is a significant negative predictor of in-hospital mortality for patients with ET≤12 h.

Effective surgical treatment for controlling the acute heart failure induced by acutely progressed mitral regurgitation with nonbacterial thrombotic endocarditis.

A 45-year-old woman complaining of consciousness disturbance demonstrated multiple brain infarctions. Echocardiogram showed vegetation on the posterior mitral leaflet. Infectious endocarditis was initially suspected and we started empirical antibiotics. However, mitral vegetation grew rapidly and caused severe mitral regurgitation. Acute heart failure was so poorly controlled by conservative treatment that we concluded cardiac surgery was indicated. Mitral valve replacement was safely performed, and there was no sign of heart failure or recurrent thromboembolism during the postoperative course. Thereafter, multiple hepatic masses and a solid lesion in the pancreatic head were detected by computed tomography. The patient finally died of multiple organ failure that presumably resulted from malignancy in the terminal stage. The clinical course of this case can be explained by the pathology of nonbacterial thrombotic endocarditis (NBTE). The standard treatment for NBTE consists of systemic anticoagulation as well as controlling the underlying malignancy. However, we could not diagnose this case as NBTE before surgery. Although mitral valve replacement was finally effective to control acute heart failure in this case, NBTE should be exactly diagnosed as quickly as possible and the treatment policy should be deliberated.

Pulmonary hemorrhage in a middle-aged woman as a complication of treatments for acute myocardial infarction.

A 49-year-old woman complaining of anterior chest pain underwent emergent coronary angiogram and thrombotic obstruction in the proximal left anterior descending artery was discovered. Deployment of a bare metal stent recovered good coronary flow and congestive heart failure was soon relieved. However, on day 3 of hospitalization, chest radiography suddenly showed newly emergent bilateral pulmonary infiltration shadow mimicking congestive heart failure. Chest computed tomography and clinical findings suggested bilateral alveolar hemorrhage. The patient received dual antiplatelet therapy, aspirin 100 mg/day and clopidogrel 75 mg/day and continuous 15,000 U/day heparin infusion, after percutaneous coronary intervention. Therapies that minimize bleeding risk while maintaining an antithrombotic effect are required for patients with acute coronary syndrome (ACS). Due to concern about the increased risk of early stent thrombosis induced by discontinuation of antiplatelet therapy, we continued to administer dual antiplatelet therapy. Pulmonary hemorrhage complicated with ACS without abciximab is a rare clinical entity, and we successfully overcame this potentially life-threatening complication with conservative therapy.

Pressure-mediated hypertrophy and mechanical stretch induces IL-1 release and subsequent IGF-1 generation to maintain compensative hypertrophy by affecting Akt and JNK pathways.

RATIONALE: It has been reported that interleukin (IL)-1 is associated with pathological cardiac remodeling and LV dilatation, whereas IL-1beta has also been shown to induce cardiomyocyte hypertrophy. Thus, the role of IL-1 in the heart remains to be determined. OBJECTIVE: We studied the role of hypertrophy signal-mediated IL-1beta/insulin-like growth factor (IGF)-1 production in regulating the progression from compensative pressure-mediated hypertrophy to heart failure. METHODS AND RESULTS: Pressure overload was performed by aortic banding in IL-1beta-deficient mice. Primarily cultured cardiac fibroblasts (CFs) and cardiac myocytes (CMs) were exposed to cyclic stretch. Heart weight, myocyte size, and left ventricular ejection fraction were significantly lower in IL-1beta-deficient mice (20%, 23% and 27%, respectively) than in the wild type 30 days after aortic banding, whereas interstitial fibrosis was markedly augmented. DNA microarray analysis revealed that IGF-1 mRNA level was markedly (approximately 50%) decreased in the IL-1beta-deficient hypertrophied heart. Stretch of CFs, rather than CMs, abundantly induced the generation of IL-1beta and IGF-1, whereas such IGF-1 induction was markedly decreased in IL-1beta-deficient CFs. IL-1beta released by stretch is at a low level unable to induce IL-6 but sufficient to stimulate IGF-1 production. Promoter analysis showed that stretch-mediated IL-1beta activates JAK/STAT to transcriptionally regulate the IGF-1 gene. IL-1beta deficiency markedly increased c-Jun N-terminal kinase (JNK) and caspase-3 activities and enhanced myocyte apoptosis and fibrosis, whereas replacement of IGF-1 or JNK inhibitor restored them. CONCLUSIONS: We demonstrate for the first time that pressure-mediated hypertrophy and mechanical stretch generates a subinflammatory low level of IL-1beta, which constitutively causes IGF-1 production to maintain adaptable compensation hypertrophy and inhibit interstitial fibrosis.

Subacutely progressed extensive aortic dissection complicated with catheter-induced dissection in left main coronary artery.

A 64-year-old man complaining of resting angina underwent emergent coronary angiogram and significant stenosis in the mid-left anterior descending artery was discovered. Although deployment of the drug-eluting Cypher stent relieved the stenosis, the guiding catheter accidentally induced coronary dissection in the left main coronary artery (LMCA). Then, deployment of another Cypher stent at the lesion successfully managed the complication. 20 days later, although asymptomatic, extensive aortic dissection was detected from the coronary sinus of Valsalva to the femoral artery. 64-Row multidetector computed tomography demonstrated that the dissection originated from the LMCA and retrogradely expanded to the aorta. This type of dissection is a rare complication related to coronary intervention and even in such a clinical setting, asymptomatic delayed progression of retrograde aortic dissection has not previously been reported to our knowledge.

Fatal splenic laceration in a young woman caused by idiopathic isolated splenic vein thrombosis.

A 38-year-old woman died of hemorrhagic shock caused by idiopathic bleeding in the abdominal cavity. At autopsy, more than 5,000 mL hemoperitoneum was detected. There was no remarkable bleeding site except for a small tear in the surface of the spleen. Microscopic examination suggested that isolated splenic vein thrombosis induced coagulative necrosis of the spleen and subsequently caused splenic laceration. Whenever a case of hemoperitoneum is encountered, splenic rupture should be included in the differential diagnosis; it is imperative to manage such cases as promptly as possible.

Spironolactone modulates expressions of cardiac mineralocorticoid receptor and 11beta-hydroxysteroid dehydrogenase 2 and prevents ventricular remodeling in post-infarct rat hearts.

Aldosterone antagonists have been reported to prevent ventricular remodeling after myocardial infarction (MI) via their action to extracellular matrix (ECM). However, it remains largely unknown whether aldosterone antagonists attenuate myocyte loss in the remodeling process. The present study examined whether spironolactone prevents myocyte apoptosis and improves post-infarct ventricular remodeling in rats. MI was achieved by permanent occlusion of the left coronary artery. Administration of spironolactone (100 mg/kg/day) was started immediately after MI. Sprague-Dawley rats were divided into four groups: 1) sham, 2) spironolactone-treated sham, 3) untreated MI, 4) spironolactone-treated MI. Echocardiographic parameters (left ventricular [LV] diastolic dimension [LVDd], fractional shortening [%FS]), hemodynamic parameters (LV systolic pressure [LVSP], LV end-diastolic pressure [LVEDP], dP/dt(max) and dP/dt(min)) and collagen accumulation quantitated by Masson's Trichrome staining were significantly improved in the spironolactone-treated MI group on the 14th day, compared with the untreated MI group. Moreover, the percentage of apoptotic myocytes evaluated by terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) assay was significantly lower in the spironolactone-treated MI group on the 2nd (3.54% vs. 5.79% in untreated MI group), 7th (0.65% vs. 1.37% in untreated MI group) and 14th days (0.11% vs. 0.16% in untreated MI group). Real time reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that the expression of mineralocorticoid receptor (MR) mRNA and that of 11beta-hydroxysteroid dehydrogenase 2 (11beta-HSD2) mRNA, which is known to confer aldosterone selectivity on MR, were upregulated in the untreated MI group, and that spironolactone significantly suppressed the expression of these genes. Moreover, spironolactone significantly inhibited aldosterone-induced apoptosis in cultured rat cardiac myocytes in a dose-dependent fashion. Our study demonstrates that, in addition to their effect on ECM, aldosterone antagonists inhibit myocyte apoptosis and prevent post-infarct ventricular remodeling by modulating the expression levels of MR and 11beta-HSD2, which are enhanced in the remodeling heart.

Nicorandil regulates Bcl-2 family proteins and protects cardiac myocytes against hypoxia-induced apoptosis.

Nicorandil has been shown to inhibit myocyte apoptosis by opening of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels and nitrate-like effect against oxidative stress. However, the detailed mechanism of nicorandil-mediated cardioprotection under hypoxic conditions remains to be largely unknown. The present study examined whether nicorandil can inhibit apoptosis via regulation of Bcl-2 family proteins in hypoxic myocytes. Neonatal rat cardiac myocytes were exposed to hypoxia for 7 hours. Hypoxia-induced myocyte apoptosis (13.9+/-0.9%) under glucose-rich conditions. Myocyte apoptosis was accompanied by loss of mitochondrial membrane potential (Deltapsi(m)), cytochrome c release from mitochondria into cytosol, and activation of caspase-3. Hypoxia also significantly increased Bax and decreased Bcl-2 mRNA and protein expression, thereby increasing Bax/Bcl-2 ratio. Nicorandil 100 micromol/l significantly decreased the percentage of apoptotic myocytes (7.2+/-0.5%) by inhibiting loss of Deltapsi(m) and translocation of cytochrome c. These effects of nicorandil were partially but significantly inhibited by cotreatment of either 500 micromol/l 5-hydroxydecanoate, a selective mitoK(ATP) channel antagonist, or 10 micromol/l 1H-[1,2,4]oxidazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase. Moreover, nicorandil significantly inhibited the hypoxia-induced changes in Bax and Bcl-2 expression, and concomitant increased Bax and decreased Bcl-2 immunoreactivity in mitochondria. These effects of nicorandil in Bax and Bcl-2 expression were significantly blunted by cotreatment of ODQ and 5-HD, respectively. Cotreatment of KT5823, an inhibitor of protein kinase G, significantly blocked the effect of nicorandil on Bax expression and 8-bromo-cyclic guanosine 3',5' monophosphate (8-bromo-cGMP), a cGMP analog, mimicked the effect of nicorandil on Bax expression. The present study demonstrates that nicorandil regulates Bcl-2 family proteins via opening of mitoK(ATP) channels and nitric oxide-cGMP signaling and inhibits hypoxia-induced mitochondrial death pathway.

[Assessment of microcirculation disturbance in patients with coronary ectasia by ATP-loading 99mTc-tetrofosmin myocardial SPECT].

UNLABELLED: Patients with coronary ectasia often develop chest pain and reveal ischemic changes on electrocardiograms and reduced left ventricular wall motion on left ventriculography, in the absence of epicardial coronary artery stenotic regions. We examined the disturbances in the coronary microcirculation in patients with coronary ectasia using left ventriculography and ATP loading 99mTc-tetrofosmin myocardial single photon emission computed tomography (SPECT) before and after administration of a coronary vasodilator and antiplatelet agents. METHODS: Twenty patients in whom coronary angiography revealed diffuse coronary artery ectasia but no stenotic regions were enrolled in this study. Left ventriculography and ATP loading 99mTc-tetrofosmin myocardial SPECT were performed before and after administration of the coronary vasodilator, nicorandil, as well as that of the antiplatelet agents, aspirin and ticlopidine. RESULTS: (1) The ejection fraction in left ventriculography was 48.3 +/- 17.4% before, and 56.6 +/- 18.3% after the drug administration, the ejection fraction was improved after the drug administration (p < 0.05). (2) Before the drug administration, the total defect scores on 99mTc-tetrofosmin myocardial SPECT were 5.9 +/- 3.1 and 8.8 +/- 2.7 in the ATP-loading and rest images, respectively (p < 0.05), and the corresponding scores after the drug administration were 4.1 +/- 3.0 and 5.4 +/- 3.1, respectively (N.S.). Thus, the total defect scores in the ATP-loading and rest images improved after the drug administration (p < 0.05). CONCLUSION: Myocardial damage in patients with coronary ectasia might be induced by microthrombotic embolism and microcirculation disturbance.

Ampulla ('takotsubo') cardiomyopathy of both ventricles: evaluation of microcirculation disturbance using 99mTc-tetrofosmin myocardial single photon emission computed tomography and doppler guide wire.

An 84-year-old woman was admitted to hospital with chest pain at rest. An electrocardiogram showed ST-segment elevation in leads II, III, aV(F) and V(2-6), and the 2-dimension echocardiogram showed apical ballooning akinesis and basal hyperkinesis of both ventricles. (99m)Tc-tetrofosmin myocardial single photon emission computed tomography (SPECT) showed severely reduced uptake in the apex. Coronary angiography did not show any organic stenosis, and epicardial coronary spasm was not provoked by the ergonovine loading test. Left ventriculography showed apical ballooning akinesis and basal hyperkinesis, which were also apparent on right ventriculography. The coronary flow velocity pattern showed rapid diastolic acceleration and deceleration times, and the coronary flow reserve measured with a Doppler guide wire was severely decreased. (99m)Tc-tetrofosmin myocardial SPECT showed improvement in the findings after 14 days, and the coronary flow velocity pattern and coronary flow reserve improved after 30 days. Left and right ventriculography both revealed mild improvement in the wall motion. These findings suggested that a microcirculation disturbance caused ampulla ('Takotsubo') cardiomyopathy.

Aldosterone directly induces myocyte apoptosis through calcineurin-dependent pathways.

BACKGROUND: Aldosterone has recently attracted considerable attention for its involvement in the pathophysiology of heart failure, in which apoptotic cell loss plays a critical role. This study examined whether aldosterone directly induces myocyte apoptosis via its specific receptors. METHODS AND RESULTS: Neonatal rat cardiac myocytes were exposed to aldosterone (10(-8) to 10(-5) mol/L). Nuclear staining with Hoechst 33258 showed that aldosterone induced myocyte apoptosis in a dose- and time-dependent fashion. Treatment of myocytes with 10(-5) mol/L aldosterone significantly increased the percentage of apoptosis (15.5+/-1.4%) compared with serum-deprived control (7.3+/-0.6%). Radio ligand binding assay revealed the existence of plasma membrane receptor with high affinity (K(d), 0.2 nmol/L) for aldosterone in cardiac myocytes but not in fibroblasts. Aldosterone rapidly (approximately 30 seconds) mobilized [Ca2+]i that was blocked by neomycin. Aldosterone induced dephosphorylation of the proapoptotic protein Bad, enhancement of mitochondrial permeability transition, decrease in mitochondrial membrane potential, and release of cytochrome c from the mitochondria into the cytosol with concomitant activation of caspase-3. These effects of aldosterone were inhibited by concurrent treatment with either an L-type Ca2+ channel antagonist, nifedipine, or inhibitors for the Ca2+-dependent phosphatase calcineurin, cyclosporin A and FK506. CONCLUSIONS: The present study demonstrates for the first time that the specific plasma membrane receptor (coupled with phospholipase C) for aldosterone is present on cardiac myocytes and that aldosterone accelerates the mitochondrial apoptotic pathway through activation of calcineurin and dephosphorylation of Bad, suggesting that the proapoptotic action of aldosterone may directly contribute to the progression of heart failure.

A case of deep venous thrombosis with a double inferior vena cava effectively treated by suprarenal filter implantation.

Embryogenesis of the inferior vena cava (IVC) is a complex process involving the formation and regression of several anastomoses, thus, various anomalies may occur. We report a case of deep venous thrombosis (DVT) accompanied by a double inferior vena cava (DIVC). A 76-year-old-man was admitted because of right leg edema and pain. Venography revealed two IVC and massive venous thrombus. To avoid massive pulmonary embolism (PE), it was necessary to block both the right and the left IVC. However, the right IVC was too small to implant the filter, so we placed a temporary IVC filter (Antheor filter) in the suprarenal portion of the IVC, after the confluence of the two IVC, and started thrombolytic and anticoagulant therapy. Venography, performed 6 days after filter implantation, showed a considerable amount of remaining thrombus. We replaced the Antheor filter with a Gunther retrievable filter because the former has a catheter and is not suited for long-term use, whereas the latter can be used permanently. Two weeks after filter exchange, thrombus had decreased but remained. We therefore did not remove the Gunther filter. The patient's symptoms gradually improved in response to anticoagulant therapy, and he was discharged with no complications. The present case illustrates the importance of a correct understanding of anatomy and demonstrates the effectiveness of using a suprarenal IVC filter in DVT.

Nitric oxide-cGMP pathway is involved in endotoxin-induced contractile dysfunction in rat hearts.

The mechanisms by which endotoxemia causes cardiac depression have not been fully elucidated. The present study examined the involvement of nitric oxide (NO) in this pathology. Rats were infused with lipopolysaccharide (LPS) or saline, and the plasma and myocardial NO(2)(-) and NO(3)(-) (NOx) concentrations were measured before or 3, 6, and 24 h after treatment. The hearts were then immediately isolated and mounted in a Langendorff apparatus, and left ventricular developed pressure (LVDP) was determined before biochemical analysis of the myocardium. LPS injection effected the expression of inducible NO synthase (iNOS) in the myocardium, a marked increase in plasma and myocardial NOx levels, and a significant decline in LVDP compared with saline controls. The LPS-induced NO production and concomitant cardiac depression were most pronounced 6 h after LPS injection and were accompanied by a significant increase in myocardial cGMP content. Myocardial ATP levels were not significantly altered after LPS injection. Significant negative correlation was observed between LVDP and myocardial cGMP content, as well as between LVDP and plasma NOx levels. Aminoguanidine, an inhibitor of iNOS, significantly attenuated the LPS-induced NOx production and contractile dysfunction. Furthermore, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, an inhibitor of soluble guanylate cyclase, significantly decreased myocardial cGMP content and attenuated the contractile depression, although aminoguanidine or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one was not able to completely reverse myocardial dysfunction. Our data suggest that endotoxin-induced contractile dysfunction in rat hearts is associated with NO production by myocardial iNOS and a concomitant increase in myocardial cGMP.

[Assessment of microcirculation disturbance with nuclear cardiology in a patient with coronary ectasia: a case report].

A 69-year-old woman presented with dyspnea on exertion. Echocardiography showed dilatation and diffuse hypokinesis of the left ventricle. 99mTc-tetrofosmin myocardial SPECT showed moderately reduced uptake in the anteroseptal wall and the inferior wall on the rest images, but was improved on the ATP loading images. 123I-BMIPP myocardial SPECT showed severely reduced uptake in the anterior wall and the inferior wall. These SPECT findings suggested ischemic heart disease rather than dilated cardiomyopathy. Coronary angiography showed no organic stenosis, but diffuse coronary ectasia was noted in three vessels. Intravascular ultrasound revealed remarkable coronary ectasia, with a maximal diameter of 8.2 mm. Coronary flow velocity as measured by Doppler blood flow guide wire was remarkably reduced. Coronary spasms were not provocated by ergonovine loading test. These findings suggested that microvascular thrombi and disturbance of dilatation caused myocardial ischemia in this patient. We treated the patient with ticlopidine and nicorandil. Following treatment left ventricle wall motion, 99mTc-tetrofosmin and 123I-BMIPP myocardial SPECT findings were improved.

[Marked 99mTc-PYP myocardial accumulation immediately after reperfusion in a patient with acute myocardial infarction].

We reported a case of a 72-year-old man with chest pain. An electrocardiogram showed ST segment elevation in I, II, III, aVL, aVF and V1-6 leads. 99mTc-tetrofosmin myocardial SPECT showed defect in the anterior, septal, apical and inferior walls. Coronary angiography showed 99% stenosis of the proximal right coronary artery and total occlusion of the midsegment of the left anterior descending coronary artery. Therefore, direct PTCA was performed for each lesion to achieve reperfusion. We didnt's see reperfusion injury during PTCA of the left coronary artery. On the other side, we saw severe reperfusion injury, such as slow-flow, arrhythmia and falling blood pressure during PTCA of the right coronary artery. After four hours, 99mTc-PYP myocardial SPECT showed marked uptake in the apical and inferior walls, and mild uptake in the anterior and posterior walls. After three days, severely-reduced uptake of 99mTc-PYP in the apex was noted, and mild uptake in the mid-portion of the anterior wall and the mid-portion of the inferior wall. Though reperfusion injury was seen, three was mild myocardial uptake of 99mTc-PYP in the area of the right coronary artery. On the other side, despite no reperfusion injury, there showed marked uptake during the acute phase and defect during the subacute phase in the area of the left coronary artery. Wall motion of the left ventricle was normal in the area of the right coronary artery and akinesis was seen on the left. These findings suggest that 99mTc-tetrofosmin and 99mTc-PYP myocardial SPECT are useful for visualization of reperfusion injury during the acute phase and for estimation of function during the chronic phase, better even than electrocardiogram or coronary angiography.

[Efficacy of integrated backscatter imaging by acoustic densitometry for identifying ultrasonic tissue characterization of left ventricular thrombus: two case reports].

Echocardiography demonstrated a high echoic lesion(6 x 5 mm) in the apex of the left ventricle of a 72-year-old man(Case 1) and similar lesions(7 x 6 mm and 4 x 3 mm) in the apex of the left ventricle of a 60-year-old man(Case 2). The amplitude of cyclic variation of integrated backscattering of the high echoic lesions was measured by acoustic densitometry to be lower than that of the myocardium in Case 1, but similar to that of the myocardium in Case 2. Contrast echocardiography detected the perfusion defect of the high echoic lesion in Case 1, but not in Case 2 in the apical four-chamber view. These findings showed that the high echoic lesion indicated thrombus in Case 1, and papillary muscle in Case 2. Measurement of the amplitude of the time intensity curve with contrast echocardiography showed that the amplitude of thrombus was different from that of myocardium. This method is useful for ultrasonic tissue characterization.