Japanese heart journal最新文献

Exercise Q, R, and S wave amplitude changes, called the QRS score, have been reported to be a marker of exercise-induced myocardial ischemia. Therefore, in this study, using the exercise QRS score, we sought to determine if slow coronary flow (SCF) phenomenon is associated with the exercise-induced myocardial ischemia. This retrospective study included 23 patients evaluated for suspected coronary artery disease and found to have SCF (group I) and 19 subjects with angiographically-defined significant coronary artery stenosis (group II). All study subjects underwent treadmill exercise testing using the modified Bruce protocol. For each subject the amplitude of the Q, R, and S waves in leads aVF and V5 was measured manually using calipers before and immediately after exercise. The QRS score was calculated by subtracting the Q, R, and S wave differences in leads aVF and V5. There was no difference between the two groups with respect to demographic properties. The peak heart rate achieved, baseline and peak systolic-diastolic blood pressure, exercise duration, and the metabolic equivalent values were similar in both groups. The maximum ST-segment depression ratio was significantly lower in patients with SCF than those of significant coronary stenosis (0.8 +/- 0.4 vs 1.3 +/- 0.5 P = 0.001, respectively). However, the exercise QRS score was found to be similar in both groups (3.3 +/- 2.3 vs 2.1 +/- 3.0 P = 0.2, respectively). The data suggest that SCF phenomenon may alone lead to myocardial ischemia even in the absence of obstructed major epicardial coronary arteries as detected by similar exercise QRS scores to those of significant coronary artery stenosis.

Chylous ascites is a clinical entity characterized by accumulation of milky fluid containing high amounts of triglycerides in the peritoneal cavity. The cause is usually lymphatic obstruction secondary to neoplastic processes. Constrictive pericarditis rarely causes cylous ascites through elevated venous pressure and lymphatic stasis. To the best of our knowledge, there is no report of constrictive pericarditis leading to chylous ascites in a patient presenting with objective lymphangiographic findings of lymphatic obstruction rather than stasis. We present a case of chylous ascites and pleural effusion secondary to constrictive pericarditis presenting with signs of lymphatic obstruction in lymphangio-graphy, in whom complete clinical and laboratory improvement was achieved after pericardiectomy.

Unlabelled: Lipoprotein (a) (Lp(a)) is an independent risk factor for myocardial infarction (MI). It may also inhibit the fibrinolysis system, and Lp (a) affects the natural course of MI and the results of thrombolytic therapy. The purpose of this study was to investigate the influence of Lp (a) on the residual lesion stenosis of the infarction-related arteries (residual stenosis) in acute MI patients in whom reperfusion therapy was not performed. We studied 129 MI patients not given reperfusion therapy who underwent coronary angiography in the chronic stage. Morning fasting blood was collected and Lp (a), blood sugar, total cholesterol (TC), triglycerides (TG), and hemoglobin A1c (HbA1c) were measured. Residual stenosis was compared between the low Lp(a) group (< 30 mg/dL) and the high Lp(a) group (> or = 30 mg/dL). It was severe in the high Lp(a) group (85.0 +/- 24.9% vs 94.5 +/- 15.5%, P = 0.0044). We also compared residual stenosis and TIMI classification between younger and older, non-DM and DM, non-HT and HT, low-TC (< 220 mg/dL) and high-TC (> or = 220 mg/dL), low-TG (< 150 mg/dL) and high-TG (> or = 150 mg/dL), and low-Lp (a) and high-Lp (a) patients. Only the serum Lp (a) level affected the residual stenosis and TIMI classification (P < 0.05).

Conclusion: These findings suggest that elevated Lp (a) levels inhibit fibrinolysis.

Mitral annulus calcification (MAC) is a chronic degenerative noninflammatory process. The goal of this study was to determine endothelin-1 (ET-1) and nitric oxide (NOx) levels in patients with MAC and compare them with those in normal subjects. The study group included 39 patients [26 females (66%), age, 63 +/- 8 years] with MAC and 20 [11 females (55%), age, 61 +/- 7 years] healthy subjects. The patients were divided into two subgroups, group A with severe MAC and group B with mild MAC, according to the severity of the MAC. Plasma ET-1 levels were higher and NOx levels were lower in patients than controls [(6.5 +/- 5.6 pg/mL vs 3.7 +/- 2.9 pg/mL for ET-1 and 35.0 +/- 10.6 micromol/L vs 42.3 +/- 9.9 micromol/L for NOx; P < 0.05 for both)]. In the subgroups, ET-1 levels were higher in group A than group B (8.65 +/- 6.84 pg/mL vs 4.74 +/- 3.45 pg/mL, P < 0.05) and the control group (8.65 +/- 6.84 pg/mL vs 3.70 +/- 2.88 pg/mL, P < 0.05). There was no difference between group B and the control group. Plasma NOx levels were significantly decreased in group A compared to controls (32.22 +/- 11.88 micromol/L vs 42.25 +/- 9.99 micromol/L, P < 0.05). However, no significant difference was observed between group B (37.38 +/- 9.06 micromol/L) and the other groups. Diabetes mellitus, coronary artery disease, and dyslipidemia were significantly associated with ET-1 levels. However, this association was not observed for NOx. In conclusion, patients with MAC have increased ET-1 and decreased NOx levels. This seems to be more prominent in patients with severe MAC.

In patients with end stage renal disease on hemodialysis (HD), left ventricular (LV) function is frequently impaired. However, the mechanism of the LV dysfunction is totally unknown. It has been suggested that overproduction of nitric oxide induced by inflammatory cytokines may contribute to the LV dysfunction in some diseased states. In this study, we examined whether inflammatory cytokines play a role in the altered LV function in HD patients. The plasma concentrations of 5 major inflammatory cytokines, including interleukin (IL)-1alpha, IL-1beta, IL-6, tumor necrosis factor-alpha, and macrophage-colony stimulating factor (M-CSF) were measured by enzyme immunoassay with horseradish peroxidase in 18 consecutive patients on HD and in 16 control subjects. Then, we examined the relationship between plasma concentrations of M-CSF and LV ejection fraction (EF) on echocardiography. Among the inflammatory cytokines examined, only the plasma concentrations of M-CSF were significantly elevated in patients on HD as compared to the control subjects. There was no significant change in the M-CSF concentrations before and after HD. Furthermore, there was a significant negative correlation between the plasma concentrations of M-CSF and LVEF. These results suggest that elevated levels of plasma M-CSF may exist prior to the development of LV dysfunction observed in HD patients.

There is substantial evidence indicating that endogenous opioid peptides are involved in the pathophysiology of myocardial ischemia and reperfusion. We measured the myocardial and peripheral concentrations of beta-endorphin before and following myocardial ischemia and reperfusion during coronary angioplasty. The results indicate that in patients with coronary artery disease, there was an augmented myocardial concentration of beta-endorphin. Moreover, there was an increased peripheral concentration of beta-endorphin following myocardial ischemia and reperfusion. The data support the previous notion that endogenous opioid peptides are involved in the pathophysiology of ischemic heart disease.

A 62-year-old man with hypertension and hypercholesterolemia was referred to our unit for evaluation of chest pain. A very rare variant of single coronary artery, in which the anomalous right coronary artery originated as a separate branch from the left anterior descending artery, was incidentally found on his coronary angiography. The anomalous right coronary artery in our case appears to be unique in that it courses intraseptally rather than rightwards proximally and has obstructive atherosclerotic lesions resulting in inferior ischemia. Moreover, the acute angle made by the anomalous right coronary artery to turn toward the atrioventricular groove may have reduced the flow velocity and contributed to the development of inferior ischemia.

Existing indices of coronary conductance (hyperemic flow-versus-pressure slope index, FPSI, and zero flow pressure, Pzf) have been developed as measures of microcoronary resistance. These indices, however, refer to cases of normal hearts, and there are no reports studying these indices following acute myocardial infarction. In this study, we investigated whether FPSI and Pzf truly measure the extent of myocardial salvage after successful reperfusion therapy. We also developed a new index of zero pressure flow, Fzp. Nineteen patients who underwent successful reperfusion therapy to the proximal portion of the left anterior descending artery (LAD) were studied. After successful reperfusion therapy, a Doppler wire was placed into the LAD. Aortic pressure was recorded in real time. Results from the aortic pressure and flow meter were combined to produce FPSI, Pzf, and Fzp. All cases underwent a resting thallium (Tl) and BMIPP scintigram within five days of successful reperfusion therapy. Infarcted myocardium was estimated using a severity score calculated from the Tl scintigraphy (TlSS), and the BMIPP (BMIPPSS) was estimated using a severity score. Patients with a TlSS/BMIPPSS ratio of less than 0.4 were assigned to the successful salvage group (group S), while the others were assigned to the failed salvage group (group F). FPSI of group F was 1.91 +/- 0.26 m/sec and of group S was 0.92 +/- 0.43 m/sec (P < 0.01). Pzf of group F was 51 +/- 3 mmHg and of group S was 51 +/- 5 mmHg (NS). Fzp of group F was -98 +/- 16 cm/sec and of group S was -46 +/- 4 cm/sec (P < 0.05). FPSI and the new index of Fzp were useful in estimating the extent of myocardial salvage. Our results suggest that the Pzf index could not differentiate between the two groups.

A 60-year-old male with exertional dyspnea was referred to our hospital. Right pulmonary artery stenosis due to external compression by a calcified band was diagnosed by echocardiography, computed tomography, and magnetic resonance imaging. Percutaneous transluminal angioplasty was conducted in vain due to vascular recoil and failure of stent delivery. Pulmonary bypass grafting was performed successfully. The surgery indicated a probable etiology of chronic pericarditis. This is an extremely rare case of adult pulmonary artery stenosis without a known history of congenital disease, constrictive pericarditis, tuberculosis, or surgery.

Cases with cardiac hydatid cyst disease are uncommon, being approximately 0.2-2% of all cases. Most cardiac hydatid cysts are located in the interventricular septum or left ventricular wall. Pericardial location is very rare. We report a 42-year old Turkish man with pericardial hydatid cyst disease who was otherwise asymptomatic, having no cardiac symptomatology. The most appropriate therapeutical option for a hydatid cyst is surgical removal of the cyst mass. However, our patient refused surgical treatment and thus medical treatment with albendazole was initiated. Following the first month of the drug therapy, pericardial effusion disappeared. The cystic nature of the mass disappeared and was solidified at the 6th month of treatment. The patient has been followed-up by us asymptomatically.