Assessment of platelet-derived thrombogenicity with the total thrombus-formation analysis system in coronary artery disease patients receiving antiplatelet therapy.

BACKGROUND: Accurate evaluation of thrombogenicity helps to prevent thrombosis and excessive bleeding. The total thrombus-formation analysis system (T-TAS) was developed for quantitative analysis of platelet thrombus formation by the use of microchips with thrombogenic surfaces (collagen, platelet chip [PL-chip]; collagen plus tissue factor, atherome chip [AR-chip]). We examined the utility of the T-TAS in the assessment of the efficacy of antiplatelet therapy in patients with coronary artery disease (CAD). METHODS AND RESULTS: In this cross-sectional study, 372 consecutive patients admitted to the cardiovascular department were divided into three groups: patients not receiving any antiplatelet therapy (control, n = 56), patients receiving aspirin only (n = 69), and patients receiving aspirin and clopidogrel (n = 149). Blood samples were used for the T-TAS to measure the platelet thrombus-formation area under the curve (AUC) at various shear rates (1500 s(-1) [PL18 -AUC10 ] and 2000 s(-1) [PL24 -AUC10 ] for the PL-chip; 300 s(-1) [AR10 -AUC30 ] for the AR-chip). The on-clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system. The mean PL24 -AUC10 levels were 358 ± 111 (± standard deviation) (95% confidence interval [CI] 328.9-387.1) in the control group, 256 ± 108 (95% CI 230.5-281.5) in the aspirin group, and 113 ± 91 (95% CI 98.4-127.6) in the aspirin/clopidogrel group. In the aspirin/clopidogrel group, the PL24 -AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 ± 112, 95% CI 103.4-200.6) than in the non-PM group (87 ± 74, 95% CI 73.8-100.2). CONCLUSIONS: Our findings suggest that the PL24 -AUC10 level measured by the T-TAS is a potentially suitable index for the assessment of antiplatelet therapy in CAD patients.

Aldehyde dehydrogenase 2 as a potential protective factor for renal insufficiency in Japanese subjects with heart failure: a pilot study.

The association between the aldehyde dehydrogenase 2 (ALDH2, rs671) genotypes and the estimated glomerular filtration rate (eGFR) was investigated in Japanese hypertensive patients with/without coronary artery disease or with ischemic heart failure (HF), and age/sex-matched normotensive healthy controls. The eGFRs were significantly lower in the HF subjects with the ALDH2 *2/*2 genotype than in those with the other genotypes. Multiple regression analyses adjusted by the potentially confounding factors showed the *2/*2 genotype to be significantly associated with the decreased eGFR, compared to the *1/*1 genotype (ß = 31.99 ml min1 per 1.73 m2, P < 0.01).

Induction of the histidine decarboxylase genes of Photobacterium damselae subsp. damselae (formally P. histaminum) at low pH.

AIMS: To elucidate the detailed mechanism of histamine production by Photobacterium damselae subsp. damselae. METHODS AND RESULTS: Histidine decarboxylase and related genes of P. damselae subsp. damselae were cloned, and three open reading frames named as hdcT, hdcA and hisRS were identified. The hdcA gene encodes a polypeptide of 377 amino acids and is considered to be the pyridoxal-P dependent histidine decarboxylase. The hdcT gene is assumed to be a histidine/histamine antiporter, and the hisRS gene is considered to be a histidyl-tRNA synthetase. Recombinant Escherichia coli strains harbouring plasmids carrying the P. damselae hdc genes were shown to over-excrete histamine extracellularly. Northern blot analysis and quantitative RT-PCR revealed high levels of mono- and bi-cistronic transcripts of hdcA, hdcT and hisRS genes under conditions of low pH and histidine excess. CONCLUSIONS: The hdcA gene of P. damselae was constructed as an operon with putative histidine/histamine antiporter and histidyl-tRNA synthetase. Mono- and poly-cistronic transcripts and acid induction were detected. SIGNIFICANCE AND IMPACT OF THE STUDY: This is the first report of cloning the histidine decarboxylase gene cluster in gram-negative bacteria. Also, these genes were induced under acidic conditions and in the presence of excess histidine.

Combined revascularization strategy for acute myocardial infarction in patients with intracoronary thrombus: preceding intracoronary thrombolysis and subsequent mechanical angioplasty.

Thrombus in the infarct-related artery is one of the limitations for flow restoration in primary percutaneous transluminal coronary angioplasty (PTCA) treatment for acute myocardial infarction (AMI). The present study investigated the benefit of preceding intracoronary thrombolysis (ICT) by retrospectively analyzing acute phase flow restoration in 80 AMI patients with intracoronary thrombus: 40 undergoing primary PTCA alone (primary PTCA group) and 40 treated with preceding ICT plus PTCA (combined group). Acute phase Thrombolysis in Myocardial Infarction (TIMI) grade flow was as follows: TIMI 0/1: 35.0% vs 12.5% for the primary PTCA group and the combined group, p=0.06; TIMI 2: 7.5% vs 15.0%, p=NS; TIMI 3: 57.5% vs 72.5%, p=NS). In the subgroup analysis, it was also less in the combined group among 33 patients with a left anterior descending coronary artery (LAD) lesion (42.1 % vs 7.1%, p=0.08), but not among the remaining 47 with either a right coronary artery or left circumflex artery lesion. The combined therapy may potentially provide better acute phase flow restoration in AMI patients with an intracoronary thrombus in a LAD lesion.

Plasma monocyte chemoattractant protein-1 antigen levels and the risk of restenosis after coronary stent implantation.

Monocyte chemoattractant protein-1 (MCP-1) plays a fundamental role in monocyte recruitment and has been implicated in atherosclerosis. The present study tested the hypothesis that increased levels of MCP-1 are associated with an increased risk for restenosis post stent implantation. The plasma MCP-1 antigen levels were measured pre-stenting, and at 24 and 48 h and 6 months post stenting in 41 patients with stable exertional angina (SEA) who had undergone successful stent implantation. Nineteen patients with chest pain syndrome were selected as a control group. Initial plasma MCP-1 antigen levels (mean +/- SE, pg/ml) in the patients with SEA were significantly higher than those in the control group (852.3+/-51.4 vs 418.2+/-26.7, p<0.001). The patients with SEA were divided into 2 groups based on follow-up angiographic findings: 17 patients with restenosis (R group); 24 patients without restenosis (N group). The lesion was significantly longer in the R group than in the N group (p<0.03). Plasma MCP-1 antigen levels at pre-stenting were not significantly different between the 2 groups (820.6+/-69.1 in the R group vs 874.7+/-73.8 in the N group). Serial changes of plasma MCP-1 levels were plotted as percent changes from the initial levels (mean +/- SE, %) and were significantly higher in the R group than in the N group at 48 h and at 6 months post stent implantation (104.6+/-4.8 vs 89.2+/-3.4, p<0.01, 109.6+/-11.2 vs 98.5+/-5.0, p<0.05). The study concludes that MCP-1 production at stented coronary arterial sites is associated with an increased risk for restenosis post stent implantation.

Pulse infusion thrombolysis (PIT) for large intracoronary thrombus: preventive effect against the 'no flow' phenomenon in revascularization therapy for acute myocardial infarction.

Because large thrombus is a limitation for revascularization in acute myocardial infarction (AMI), the present study evaluated the effectiveness of pulse infusion thrombolysis (PIT) in patients with an AMI with a large (>15 mm) coronary thrombus, focusing on the occurrence of the 'no flow' phenomenon. The retrospective study compared patients treated before (1988-95; Group A, n=74) and after (1996-99; Group B, n=40) the use of PIT, using the following parameters: lesion success (<50% stenosis during 30-min observation), procedural success (lesion success plus TIMI grade 3 flow), procedural no flow (TIMI grade 0 flow during the procedure with 'back and forth movement' of contrast dye after lesion success), persistent no flow (consistent no flow without any flow improvement at the final visualization despite intensive treatment), reocclusion rate and in-hospital death. Group B was significantly better than Group A in procedural success (90% vs 66%; p=0.005), procedural 'no flow' (51% vs 15%; p<0.001), and persistent 'no flow' (34% vs 10%; p<0.05). Subgroup comparison was performed among the following groups: Direct-BA group (n=44): treated with mechanical angioplasty alone; ICT-BA group (n=40): treated with prior intracoronary thrombolysis and angioplasty; and PIT-BA group (n=30): treated with PIT and angioplasty. There were no differences in thrombus length and lesion success among these 3 groups. Procedural success was best achieved in PIT-BA: 97% vs 52% for Direct-BA (p=0.003) and 68% for ICT-BA (p=0.009). Procedural 'no flow' was least in PIT-BA: 50% vs 3.3% for Direct-BA (p=0.003) and 25% vs 3.3% for ICT-BA (p=0.042). Persistent 'no flow' was less frequent in PIT-BA than Direct-BA: 32% vs 3.3% (p=0.009). However, the difference between ICT-BA and Direct-BA was insignificant: 13% vs 3.3% (p=0.53). There were no differences in reocclusion rate and in-hospital death among the 3 subgroups. And there were no differences between Direct-BA and ICT-BA in any parameters. PIT was effective in preventing 'no flow' in the mechanical revasculalization for AMI especially those cases with a large thrombus.

Increased plasma antigen levels of monocyte chemoattractant protein-1 in patients with restenosis after percutaneous transluminal coronary angioplasty.

Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the progression of atherosclerosis in coronary arteries. To examine whether or not plasma antigen levels of MCP-1 are related to restenosis after percutaneous transluminal coronary angioplasty (PTCA), the plasma antigen levels of MCP-1 were measured by enzyme-linked immunosorbent assay (pg/ml) before, 24 and 48 h, and 3 months after elective PTCA for stable exertional angina performed between June 1997 and March 1998. Restenosis was defined as recurrence of stenosis greater than 50% of the diameter in the dilated segment at 3-month follow-up angiography. There were no differences in plasma MCP-1 antigen levels before and at 24 h after PTCA between restenosis (R; n=27) and no-restenosis (N; n=43) groups (R vs N: 633+/-35 vs 589+/-34, and 669+/-41 vs 575+/-36 pg/ml before and at 24 h after PTCA, respectively), but plasma MCP-1 antigen levels were higher at 48 h and 3 months after PTCA in the R than in N group (R vs N: 678+/-41 vs 558+/-35, and 735+/-35 vs 571+/-32 pg/ml at 48 h and 3 months after PTCA, respectively). These data suggest that the MCP-1 production and macrophage accumulation in the balloon-injured site is partially associated with restenosis after PTCA.

Photobacterium histaminum Okuzumi et al. 1994 is a later subjective synonym of Photobacterium damselae subsp. damselae (Love et al. 1981) Smith et al. 1991.

The type strain of Photobacterium histaminum, JCM 8968T (= ATCC 51805T), and that of Photobacterium damselae subsp. damselae, ATCC 33539T, exhibit 100% identity in their 16S rRNA sequence, more than 80% DNA-DNA homology and only one phenotypic difference. Also, like P. histaminum, P. damselae subsp. damselae was shown to excrete a large amount of histamine when cells were grown on medium containing excessive histidine under acidic conditions. Therefore, the name P. histaminum should be considered to be a later subjective synonym of P. damselae subsp. damselae.

Relation between coronary thrombus and angiographic no-flow during primary angioplasty in patients with acute myocardial infarction.

No flow is an unsolved issue in primary percutaneous transluminal coronary angioplasty (PTCA) for patients with acute myocardial infarction (AMI), and the pathophysiology of no-flow is undetermined. To evaluate the potential participation of coronary thromboembolism in no-flow during primary PTCA, the present study reviewed cinefilms of 256 consecutive patients who underwent primary PTCA for AMI within 24h after the onset of chest pain between January 1992 and June 1998, focusing on the thrombus size. Angiographic no-flow was defined as the cessation of flow into the distal coronary circulation of the treated vessel with a to-and-fro contrast movement, not attributable to high-grade stenosis or spasm of the original target lesion. The coronary thrombus size was determined by using the 2-cm balloon catheter as a reference after crossing the infarct-related occluded artery with a guide wire. Angiographic no-flow was observed in 37 patients (37/256, 14%): 14 of 29 cases (48%) with a large thrombus (> or =2cm) versus 23 of 227 cases (9%) with a small thrombus (<2cm, 14/29 vs 23/227, p<0.01). Among 37 patients who experienced angiographic no-flow, overt distal emboli were observed in 14 patients. A thrombolytic agent was used through a guiding catheter in 102 cases prior to or after balloon dilatation to prevent or attenuate distal embolism, particularly in all those cases with a large thrombus (29/29 100%), and angiographic no-flow was seen in 27 cases of this subgroup (27/102, 26%). It is suggested that distal thromboembolism plays an important role in the mechanism of angiographic no-flow during primary PTCA performed for AMI.

Cardiac angiotensin-converting enzyme activity in myocardial infarction.

The cardiac renin-angiotensin system is regarded as an important modulator in the infarct heart. Little is known about their presence and regulation in human hearts. We measured angiotensin-converting enzyme (ACE) and renin activities at the aortic root and anterior interventricular vein (AIV) in 51 patients with previous myocardial infarction (MI): anterior wall MI in 31 and inferior wall MI in 20 and 33 control subjects. In the anterior wall MI group, the serum ACE activity was increased significantly in the AIV than in the aortic root (16.2 +/- 5.3 vs 15.3 +/- 5.0 nmol/min/ml, p <0.001), whereas the activity was not different between the aortic root and AIV in the control (14.4 +/- 3.7 vs 14.4 +/- 3.7 nmol/min/ ml) and in the inferior wall MI (16.5 +/- 4.8 vs. 17.0 +/-5.2 nmol/min/ml) groups. On the other hand, there was no significant difference in plasma renin activity between the AIV and aortic root in the 3 groups (control group, 1.0 +/- 0.5 vs 1.0 +/- 0.5 pg/ml/hour; anterior wall MI group, 1.3 +/- 0.8 vs 1.3 +/- 0.8 pg/ml/hour; inferior wall MI group, 1.2 +/- 0.7 vs 1.3 +/- 0.8 pg/ml/ hour). The difference in serum ACE activity between the AIV and aortic root had a significant positive linear correlation with pulmonary capillary wedge pressure (r = 0.606, p <0.001), and had a significant negative linear correlation with left ventricular ejection fraction (r = -0.620, p <0.001) in the anterior wall MI group. Serum ACE activity from the infarct region of the left ventricle was augmented in patients with MI, and the activity was increased in proportion to the severity of left ventricular dysfunction.

Outcome of target sites escaping high-grade (>70%) restenosis after percutaneous transluminal coronary angioplasty.

This study examined the fate of target sites that escaped high-grade restenosis (> or = 70% diameter narrowing) after percutaneous transluminal coronary angioplasty. Although favorable long-term prognosis after successful percutaneous transluminal coronary angioplasty is well documented, little is known about the stability of target sites. Long-term follow-up (mean 6.5 years, range 1.0 to 12.0) was performed in 693 patients with 948 narrowings (stenosis <70% in diameter at follow-up coronary angiography). Among them, 249 patients (36%) with 303 target sites received late follow-up coronary angiography. The relation of target sites to the culprit lesions for coronary events or newly developed angina was angiographically reviewed and progression/regression was also examined, focusing on the target sites. Regression was observed in 16 of 255 target sites in subjects with <50% stenosis and in 21 of 48 sites in the group with midgrade stenosis of 50% to 69% luminal narrowing (16 of 255, 6.3% vs 21 of 48, 43.8%, p <0.001). Progression was observed in 33 and 4 sites (33 of 255, 12.9% vs 4 of 48, 8.3%; p = NS) in each group, respectively. The rest remained within the same range of stenosis. Culprit lesions for 2 acute myocardial infarctions, 7 unstable anginas, and 17 newly developed anginas were related to the original target sites. Three lesions developed in the midgrade stenosis group. Those 26 lesions were a component of 8.6% of 303 angiographically confirmed sites and 2.7% of total target sites. Target sites that escape high-grade restenosis frequently regress and become stable plaques and rarely trigger coronary events.

Percutaneous transluminal coronary angioplasty, alone or in combination with urokinase therapy, during acute myocardial infarction.

To investigate the effect of pre-treatment of a thrombus with a low dose of urokinase on establishing patency in a persistent infarct-related artery (IRA) during direct percutaneous coronary angioplasty (PTCA), the frequency of acute restenosis during direct PTCA, alone, or in combination with the intracoronary administration of urokinase, was examined in a consecutive nonrandomized series of patients with acute myocardial infarction (AMI). Two hundred and seventy-two successful PTCA patients (residual stenosis <50%) were divided into 2 groups: 88 patients received pre-treatment with intracoronary urokinase following PTCA (combination group); 184 received only direct PTCA without thrombolytic therapy (PTCA group). In the present study, after achievement of a residual stenosis of less than 50%, IRA was visualized every 15 min to assess the frequency of acute restenosis, which was defined as an acute progression of IRA with more than 75% restenosis after initially successful PTCA. In the patients with a large coronary thrombus, the frequency (times) of acute restenosis was significantly lower in the combination group than in the PTCA group (0.98+/-0.19 vs 2.92+/-0.32, p<0.0001). On the other hand, in the patients with a small coronary thrombus, the frequency of acute restenosis showed no difference in either group. The present study indicates that in patients with AMI, PTCA combined with pre-treatment of a low dose of urokinase is much more effective than PTCA alone, especially for those patients who have a large coronary thrombus.

Evaluation of new 4 French catheters by comparison to 6 French coronary artery images.

The use of 4 Fr catheters for diagnostic coronary arteriography improves patient comfort and could potentially reduce costs by decreasing arterial complications and encouraging outpatient examination. We examined the performance of recently developed 4 Fr catheters (100 cm long, 0.042 inch internal diameter) through in vitro flow rate patterns and in vivo image quality. Flow patterns (flow rate calculated from pressure with the Hagen Poiseuille relation) were obtained by hand (10 ml volume; maximal effort, one-handed full injection) and power injection (10 ml volume; 5 ml/sec) in the 4 Fr catheters were compared to 5 Fr (0.047 inch) and 6 Fr (0.057 inch) catheters. In 20 patients, coronary arteriograms were obtained from 4 Fr hand injection (4 HI), 4 Fr power injection (4 PI), 6 Fr hand injection (6 HI ), and 6 Fr power injection (6 PI) were compared after being scored into 5 grades. Coronary diameter was assessed at two sites for all injections in the same group of patients. In power injections, peak flow rates were consistently 5.5 ml/sec in all catheters. Hand injections were much more variable; peak flow rate ranges for 5 different physicians were 3.5-6.0 ml/sec. in 6 Fr, 1.8-3.0 ml/sec. in 5 Fr and 1.4-2.0 ml/sec in 4 Fr catheters. Mean image scores of left arteriograms were significantly higher for 4 PI versus 4 HI and for 6 Fr images compared to 4 PI (p < 0.001). In right arteriograms, 4 HI scored significantly lower than other methods (4 PI, 6 HI and 6 PI; p < 0.001). In 4 HI left coronary arteriograms, the frequency of grade > 2 was 96% and > 3 was 82%. Power injection improved 4 Fr imaging to 99% greater than grade 2 and 93% greater than grade 3. There were no differences in the frequency of images above grade 3 in right coronary arteriograms. Measured coronary artery diameters at 40 normal and 17 stenotic sites by QCA analysis (Acom, Siemens AZ, Erlangen, Germany) did not influence the study data. We concluded that coronary arteriograms by hand injection with 4 Fr catheters were inferior compared to 6 Fr images. Power injection and/or larger catheters may be necessary to ensure the highest quality images are obtained.

A comparison of the food composition table-based estimates of dietary element intake with the values obtained by inductively coupled plasma atomic emission spectrometry: an experience in a Japanese population.

In order to make quantitative comparison between food composition table-based estimates and instrumental measures by inductively coupled plasma atomic emission spectrometry (ICP-AES), total food duplicates were collected from 232 adult women in 10 study regions in 9 Prefectures in Japan. Daily dietary intake of 5 elements, sodium (Na), potassium (K), phosphorus (P), calcium (Ca) and iron (Fe), were estimated from the weights of food items in each duplicate by use of food composition tables. Parallel to this the intakes were measured by wet-ashing of food duplicate homogenates followed by ICP-AES analysis. Because the emission intensity of K was significantly modified by Na co-present at various concentrations, K was measured after Na concentration was reduced to the value 150 mg/L by dilution. The comparison of the two sets of the results, the estimated values and the measured values, showed that the estimated values were significantly larger than the measured values in the cases of Na, K, Ca and P (the ratio of the estimated to the measured values: 118% for Na, 115% for K, 109% for Ca; and 130% for Fe), whereas the two values essentially agreed with each other in the case of P (ratio: 93%). The differences were too large for any nutritional evaluation to be made when the method of Bland and Altman is applied. The significance of the differences in relation to nutritional evaluation of element intake is discussed.

Expression of angiotensin-converting enzyme in remaining viable myocytes of human ventricles after myocardial infarction.

BACKGROUND: Local ACE in the heart may be important in the pathophysiological state after myocardial infarction (MI). It is unknown, however, whether ACE is expressed in myocytes of the human heart. METHODS AND RESULTS: Using a newly generated polyclonal antibody to a synthetic peptide corresponding to part of the human endothelial ACE sequence, we examined the localization of ACE in left ventricles of patients (n = 10) with MI obtained at left ventricular aneurysmectomy or autopsy and in the hearts of control subjects at autopsy (n = 10). The avidinbiotinylated peroxidase complex method was used for the immunohistochemical staining for ACE. In the left ventricles, positively stained myocytes for ACE were found in 8 of the 10 patients with MI. ACE immunoreactivity was seen in the remaining viable myocytes located near the infarct scar of the aneurysmal left ventricle and in nonmyocytes such as fibroblasts, macrophages, vascular smooth muscle cells, and endothelial cells within the scarred tissue. On the other hand, no immunoreactivity for ACE was detected in the ventricular myocytes of all control hearts obtained at autopsy. CONCLUSIONS: We observe immunohistochemical staining for ACE in the left ventricular myocytes of the region adjacent to the infarct scar and in nonmyocytes. These results indicate that ACE is markedly increased on the edge of the infarct scar and suggest that local ACE may be important in the ventricular remodeling after MI.

Increased angiotensin converting enzyme activity in left ventricular aneurysm of patients after myocardial infarction.

OBJECTIVE: Angiotensin converting enzyme (ACE) inhibitors have been shown to improve left ventricular dysfunction and survival in patients with chronic myocardial infarction. The aim of this study was to examine the ACE activity in infarcted tissues in such patients in comparison with non-diseased tissues from control subjects obtained at necropsy. METHODS: ACE activity was measured in the left ventricles and right atrial auricles of patients (n = 9) with chronic myocardial infarction obtained at left ventricular aneurysmectomy, and in the hearts of control subjects at necropsy (n = 10). RESULTS: In non-diseased hearts, the ACE activity was highest in right atria and auricles [2.4(SEM 0.2), 2.2(0.3) nmol.mg-1 protein.min-1, NS, respectively], followed by left atria [1.7(0.2)], left auricles [1.5(0.1)], right ventricles [1.0(0.2)], and left ventricles [0.5(0.1)]. The ACE activity was significantly increased in aneurysmal tissues of patients with chronic myocardial infarction relative to left ventricles of control subjects [4.2(0.4) v 0.5(0.1) nmol.mg-1 protein.min-1, P < 0.01]. There was, however, no difference in the ACE activity of right atrial auricles between patients with chronic myocardial infarction and control subjects [2.8(0.5) v 2.2(0.3), NS]. In patients with chronic myocardial infarction, the ACE activity was higher in left ventricles than in right auricles (P < 0.01). The ACE activities in the infarcted and control ventricles were negatively correlated with the membrane protein content (r = -0.77, P < 0.01). CONCLUSIONS: In non-diseased human hearts, the ACE activity is higher in atria than in ventricles and higher in the right than in the left ventricle. Furthermore, the ACE activity in aneurysmal left ventricular tissue after myocardial infarction is higher than in non-diseased left ventricular myocardium. These results suggest that the local ACE in the human heart may play an important role in the pathophysiological state after myocardial infarction.

[A case of unilateral pulmonary edema associated rupture of mitral chordae tendineae].

A 57-year-old man was admitted with dyspnea and bloody sputum. The chest X-ray showed unilateral alveolar infiltration, and alveolar cell carcinoma was suspected. Physical examination showed orthopnea and a loud systolic murmur, and the echocardiogram showed mitral valve prolapse. A chest X-ray 4 days later revealed bilateral infiltration. The cardiac catheterization showed pulmonary congestion and the capillary wedge pressure revealed a prominent V wave. Papanicolaou's test of sputum was negative. These findings suggested heart failure due to mitral regurgitation rather than lung carcinoma. The patient underwent mitral valve replacement because of his refractoriness to the medical treatment. During the operation, the chordae tendineae of the anterior mitral leaflet was found to be completely ruptured. The mechanisms of unilateral pulmonary edema could not be ascertained, but the effect of posture and gravity was thought to be a possible mechanism.