[Show abstract][Hide abstract] ABSTRACT: Because of the unusual anatomy of an anomalous origin of the right coronary artery from the left sinus of Valsalva, selective cannulation of the guiding catheter in percutaneous coronary intervention for these cases is always challenging.
A 58-year-old Japanese man was admitted to our hospital complaining of worsening exertional chest pain. He was suspected of having unstable angina pectoris and underwent cardiac catheterization. We found a subtotal occlusive lesion in the mid-portion of his right coronary artery that originated from the left sinus of Valsalva. On the previous percutaneous coronary intervention, we failed to cannulate the guiding catheter to the anomalous orifice of the right coronary artery. Therefore, we decided to use the GuideLiner catheter for stable back-up support from the beginning. A 6Fr GuideLiner catheter was introduced into the right coronary artery by anchoring it coaxially with a semi-compliant balloon catheter. And we successfully deployed two drug-eluting stents by crossing over the posterior-descending artery. Final angiography demonstrated favorable dilatation of the target lesion, and native blood flow in the right coronary artery was completely recovered.
GuideLiner is a monorail-type "child" support catheter that facilitates coaxial guiding catheter engagement and an appropriate back-up force, achieving successful device delivery to target lesions in this kind of complex percutaneous coronary intervention.
Journal of Medical Case Reports 07/2015; 9(1):163. DOI:10.1186/s13256-015-0646-0
[Show abstract][Hide abstract] ABSTRACT: We encountered a case of chronic total in-stent occlusion which involving an abrupt-type entry at an obtuse marginal branching ostium. It is usually difficult to antegradely penetrate this kind of proximal fibrous cap. Therefore, we adopted a reverse bent wiring technique with a Crusade catheter and successfully completed all procedures. This technique is very simple but can be very effective in specific situations in daily percutaneous coronary intervention (PCI). Many PCI operators may empirically adopt this kind of wire manipulation technique. However, this kind of technique has never been officially reported to our knowledge.
[Show abstract][Hide abstract] ABSTRACT: The entrapment, fracture, and dislodgement of catheterization devices during percutaneous coronary intervention (PCI) are rare complications, for which cardiac surgery is sometimes required. Here, we encountered a rare but instructive case of balloon catheter fracture during PCI. Although there have been some reports of guidewire fracture in PCI, reports on balloon catheter fracture are very rare to our knowledge. A simulation test to examine the mechanism of balloon catheter fracture revealed that overuse of the balloon catheter, both for kissing balloon inflation and balloon anchor, was highly likely to have been the cause of the fracture.
Cardiovascular Intervention and Therapeutics 02/2015; DOI:10.1007/s12928-015-0322-8
[Show abstract][Hide abstract] ABSTRACT: Although several etiopathogenetic mechanisms have been proposed, the causes of left ventricular apical ballooning syndrome are still controversial.
A 51-year-old Japanese woman consulted the emergency room complaining of the sudden onset of anterior chest pain while shopping. We initially suspected her disease as left ventricular apical ballooning syndrome based on her clinical background and laboratory examinations. However, the initial coronary angiogram demonstrated diffuse lesions in her distal left anterior descending coronary artery, and she was finally diagnosed with apical myocardial infarction. The blood flow in her distal left anterior descending coronary artery had markedly improved in the chronic phase. If the reduced blood flow in her distal left anterior descending coronary artery was induced by coronary vasospasm and the vasospasm was relieved before the coronary angiogram was performed, this case must be diagnosed as left ventricular apical ballooning syndrome.
We think this case may promote discussion regarding the pathophysiology of left ventricular apical ballooning syndrome.
Journal of Medical Case Reports 04/2014; 8(1):124. DOI:10.1186/1752-1947-8-124
[Show abstract][Hide abstract] ABSTRACT: A 48-year-old man suffered from uncontrollable coronary vasospasms, even when taking the maximum dose of vasodilators. The patient had a history of hypereosinophilia, and as the eosinophilia worsened, more frequent and intense coronary spastic angina (CSA) attacks occurred. He was treated with 20 mg/day of oral prednisolone, and the chest symptoms of CSA completely resolved thereafter. We encountered a refractory CSA patient with an allergic predisposition for which the oral administration of corticosteroids was markedly effective. Although the priority of corticosteroid therapy is not clinically high in patients with CSA, it can be effective especially in patients with an allergic background.
Internal Medicine 04/2014; 53(7):735-8. DOI:10.2169/internalmedicine.53.1639 · 0.90 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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.
Heart and Vessels 11/2011; 28(1). DOI:10.1007/s00380-011-0210-9 · 2.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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 β-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.
International Heart Journal 01/2011; 52(3):127-30. DOI:10.1536/ihj.52.127 · 1.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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.
Journal of Cardiology Cases 10/2010; 2(2). DOI:10.1016/j.jccase.2010.03.001
[Show abstract][Hide abstract] ABSTRACT: 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.
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).
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.
Journal of Cardiology 09/2010; 56(2):204-10. DOI:10.1016/j.jjcc.2010.05.004 · 2.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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.
Journal of Cardiology Cases 02/2010; 1(1):e37-e41. DOI:10.1016/j.jccase.2009.07.003
[Show abstract][Hide abstract] ABSTRACT: 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.
Journal of Cardiology 09/2009; 54(1):128-33. DOI:10.1016/j.jjcc.2008.10.005 · 2.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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.
Internal Medicine 02/2009; 48(11):907-10. DOI:10.2169/internalmedicine.48.1843 · 0.90 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Ischemic hepatitis, otherwise known as "shock liver", is characterized by a massive, but transient increase in serum transaminase levels, usually associated with cardiac failure. A patient who did not have a predisposition to hypoglycemia was discovered at home with disturbed consciousness caused by hypoglycemia. She had been diagnosed as having constrictive pericarditis several years earlier and had developed ischemic hepatitis. Though the high serum transaminase levels were rapidly normalized, severe jaundice gradually developed and the patient finally died of multiple organ failure. Hypoglycemia, which is considered secondary to reduced gluconeogenesis in the exhausted liver, is a rare complication of constrictive pericarditis.
[Show abstract][Hide abstract] ABSTRACT: The mechanisms by which apoptotic myocytes are removed by macrophages have not been fully elucidated. This study examined whether apoptotic myocytes actively recruit macrophages by generating monocyte chemoattractant protein-1 (MCP-1) in experiments in vitro and in vivo. Neonatal rat cardiac myocytes were incubated for 4 h in the presence or absence of staurosporine (STS, 0.2-1 mumol/l), an apoptosis inducer. Nuclear staining with DAPI showed that STS induced apoptosis in a dose-dependent fashion. STS (1 mumol/l) caused extensive DNA fragmentation and increased caspase-3 activity compared with a serum-deprived control. MCP-1 mRNA and protein levels in myocytes increased twofold and fourfold, respectively, on STS treatment, and immunochemical staining revealed that apoptotic myocytes expressed MCP-1. To elucidate the role of MCP-1 expressed in apoptotic myocytes to recruit macrophages/monocytes, rat monocytes were incubated in the supernatant of STS-treated myocytes using a trans-well system. The culture medium of STS-treated myocytes recruited monocytes in a MCP-1-dependent fashion. In addition, experiments were performed in vivo using ischemia-reperfused rat hearts. Rats were subjected to 30 min of ligation of the left coronary artery followed by 24 h of reperfusion. After the reperfusion, in the ischemic border myocardium, 17.1 +/- 1.1% of myocytes were terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) positive. Moreover, double staining using the TUNEL technique and immunohistochemistry with MCP-1 antibody showed that 69.8 +/- 3.9% of TUNEL-positive myocytes expressed MCP-1 protein. Concomitantly, activated macrophages infiltrated the areas of apoptosis remarkably. These results suggest that apoptotic myocytes produce MCP-1, which have a critical role in the active recruitment of macrophages.
[Show abstract][Hide abstract] ABSTRACT: 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.
Journal of Molecular and Cellular Cardiology 05/2006; 40(4):510-9. DOI:10.1016/j.yjmcc.2006.01.020 · 4.66 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The mechanism responsible for cardiac depression in septic shock remains unknown. The present study examined whether nitric oxide (NO) overproduced by inducible NO synthase (iNOS) can inhibit aerobic energy metabolism and impair the myocardial function in endotoxin-treated rat hearts. Lipopolysaccharide (LPS) significantly decreased systolic blood pressure (BP) to 44% of control during the 48 h treatment. Hearts from control and LPS-treated rats were perfused in a Langendorff apparatus. After LPS injection, left ventricular (LV) developed pressure (LVDP) was significantly depressed, plasma NO2-/NO3- (NO(x)) concentration was markedly increased, and myocardial adenosine 5'-triphosphate (ATP), creatine phosphate (CrP), and the ratio of ATP/adenosine 5'-diphosphate were progressively decreased with time. Immunological examination showed a significant expression of iNOS protein in the LPS-treated myocytes. Aminoguanidine, an inhibitor of iNOS, significantly attenuated these LPS-induced functional and metabolic changes. Myocardial cyclic guanosine 3',5'-monophosphate (cGMP) content was significantly increased after LPS injection. Methylene blue, an inhibitor of soluble guanylate cyclase, blunted this increase in cGMP and significantly restored the LPS-induced contractile dysfunction 6 h after LPS injection. In addition, there was a significant negative correlation between LVDP and myocardial cGMP levels as well as a significant negative correlation between LVDP and plasma NO(x) levels. In contrast, 48 h after LPS injection, methylene blue no longer affected cardiac performance, and there was a significant positive correlation between LVDP and myocardial ATP content. Furthermore, the normalized activities (as a ratio of the citrate synthase activity) of mitochondrial NADH-CoQ reductase, succinate-CoQ reductase, and ATPase, were significantly inhibited, and the swelling or disruption of mitochondria cristae was seen in the 48 h LPS treatment. These LPS-induced functional and morphological disorders in the mitochondria were significantly improved by aminoguanidine. The findings suggest that sustained production of NO by iNOS leads to contractile dysfunction via cGMP in the early stage, but that it can directly impair the mitochondrial function, lower myocardial energy production, and contribute significantly to the myocardial dysfunction in the later stage of septic shock.
Journal of Molecular and Cellular Cardiology 10/2004; 37(3):775-84. DOI:10.1016/j.yjmcc.2004.06.014 · 4.66 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: 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.
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.
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.