Myocardial stunning caused by sympathetic nerve injury after an operation on cervical vertebrae.

In this case, electrocardiographic inverted T waves appeared after cervical laminaplasty and echocardiogram showed temporary wall motion abnormality. Myocardial metaiodobenzylguanidine (MIBG) uptake was obviously reduced in the same area where the wall motion abnormalities appeared in the echocardiogram, although no abnormalities were detected with myocardial thallium scintigraphy and coronary angiography. The myocardial stunning was caused by injury to the sympathetic nerves from a surgical procedure on the cervical vertebrae.

Determination of alpha-amylase using 4-O-beta-D-galactopyranosylmaltotetraose (Gal-G4) as a substrate.

A new substrate, 4-O-beta-D-galactopyranosylmaltotetraose (Gal-G4) is applied for the determination of alpha-amylase in serum and urine in a coupled assay with alpha-glucosidase (EC 3.2.1.20), glucokinase (EC 2.7.1.2) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49) as auxiliary enzymes. Gal-G4 having a 4-position of the non-reducing-end glucose residue modified by a beta-galactopyranose group is resistant for degradation by alpha-glucosidase as auxiliary enzyme. Moreover, this substrate is hydrolyzed at just one position by alpha-amylase in serum and urine. More than 99% of the products generated from Gal-G4 by alpha-amylase are identified 4-O-beta-D-galactopyranosylmaltose (Gal-G2), maltose, respectively. Glucose and maltose do not interfere the value of alpha-amylase activity at least up to 0.056 mmol/l (1 g/dl) glucose and 0.027 mmol/l (1 g/dl) maltose, respectively. We are now carrying out this work under the authority of The Enzyme committee of Japanese Society of Clinical Chemistry (JSCC) as a standard method for determination of alpha-amylase in clinical chemistry.

A prospective, randomized, double-blind multicenter trial of a single bolus injection of the novel modified t-PA E6010 in the treatment of acute myocardial infarction: comparison with native t-PA. E6010 Study Group.

OBJECTIVES: This prospective, randomized, double-blind multicenter trial evaluated the efficacy and safety of a single bolus injection of the novel modified tissue-type plasminogen activator (t-PA) E6010 in the treatment of acute myocardial infarction compared with that of native t-PA. BACKGROUND: E6010 is a novel modified t-PA with a prolonged half-life (t1/2 alpha > or = 23 min) compared with native t-PA (t1/2 alpha = 4 min). E6010 can be administered in patients as a single intravenous bolus injection, and early recanalization can be expected. METHODS: The efficacy of E6010 was compared with that of native t-PA in 199 patients with acute myocardial infarction who were treated within 6 h of onset in a prospective, randomized, double-blind multicenter trial. Patients were given either 0.22 mg/kg body weight of E6010 intravenously over 2 min or native t-PA (tisokinase) 28.8 mg or 14.4 million IU (10% of the total dose over 1 to 2 min, the remainder infused over 60 min). RESULTS: The primary end point was the recanalization rate of the infarct-related coronary artery at 60 min after the start of treatment. Time to reperfusion was shorter in the E6010 group than in the native t-PA group. Thrombolysis in Myocardial Infarction flow grade 2 or 3 recanalization at 15, 30, 45 and 60 min after administration was observed in 37%, 62%, 74% and 79% (95% confidence interval [CI] 70% to 87%) of the E6010-treated patients and in 14%, 32%, 50% and 65% (95% CI 55% to 74%) of native t-PA-treated patients, respectively (p = 0.032 at 60 min). CONCLUSIONS: The present study indicates that, compared with native t-PA, a single bolus injection of E6010 over 2 min produces a higher rate of early recanalization of the infarct-related coronary artery without fatal bleeding complications.

An index predicting coronary heart disease: LDL/HDL x 5.

Atherosclerotic changes in the coronary artery are exacerbated by the balance between LDL, which carries cholesterol into the arterial wall, and HDL, which carries it out from the wall. The molecular weight of LDL is about 2 x 10(6) and that of HDL is about 4 x 10(5), which is almost 1/5 of the molecular weight of LDL. For this reason, LDL/HDL x 5 should be a good indicator of coronary heart disease. We evaluated this index in two subject groups. At first, we determined whether it could predict the incidence of effort angina in participants of a medical examination system. Most of the subjects were healthy and good candidates for primary prevention. LDL/HDL x 5 was a more sensitive index predicting effort angina than total cholesterol, LDL or HDL. The concentrations of HDL were significantly lower in myocardial infarction patients at all ages in both sexes. The average serum concentration of HDL was 56.6 +/- 15.0 mg/dl in the medical examination group and 38.9 +/- 12.2 mg/dl in the AMI group. We tested whether our new index, LDL/HDL x 5, could predict the incidence of re-infarction in patients with myocardial infarction who were candidates for secondary prevention. LDL/HDL x 5 was a more sensitive index predicting re-infarction than total cholesterol, LDL or HDL.

Open knee dislocation associated with vascular injury successfully salvaged by primary arthrodesis in an elderly patient: a case report.

Treatment by primary arthrodesis of the knee joint after temporary intraluminal shunt placement in a 70-year-old man with open knee dislocation involving the popliteal vessels is reported. After temporary shunting, the definitive vascular reconstruction of both the popliteal artery and vein was established by end-to-end anastomoses because of the shortening effect of the arthrodesis. Two skin coverage procedures were performed on day 0 and day 18. The patient recovered activity to a level near his pretrauma status. Primary arthrodesis for open knee dislocation associated with vascular injury in an elderly patient may be an efficacious procedure, depending on the patient's age, occupation, and level of activity.

Endogenous endothelin-1 mediates cardiac hypertrophy and switching of myosin heavy chain gene expression in rat ventricular myocardium.

OBJECTIVES: We investigated the role of endogenous endothelin-1 in the development of cardiac hypertrophy in vivo under pressure overload conditions. BACKGROUND: Endothelin-1, a potent vasoconstrictor peptide, has recently been shown to act as a growth factor of myocardial cells in culture. METHODS: We examined the effect of an endothelin-A receptor antagonist (FR139317) on the development of right ventricular hypertrophy in rats with monocrotaline-induced pulmonary hypertension. Three groups of rats were studied: those given monocrotaline alone or monocrotaline plus FR139317 and those given vehicle alone (control group). RESULTS: The ratio of right ventricular systolic pressure to aortic systolic pressure was similarly elevated in rats treated with monocrotaline and monocrotaline plus FR139317. The right ventricular/left ventricular weight ratio was increased in monocrotaline-treated rats but lower in rats treated with monocrotaline plus FR139317 than in those treated with monocrotaline alone (p < 0.01). As a biochemical marker of hypertrophy, the isoform ratio of beta-myosin heavy chain protein was determined for the right ventricular tissue samples. This ratio was increased in all monocrotaline-treated rats but was lower (p < 0.01) in rats given monocrotaline plus FR139317 than in those given monocrotaline alone. The isoform ratio of beta-myosin heavy chain messenger ribonucleic acid quantitated by S1 nuclease mapping also was lower (p < 0.025) in rats receiving monocrotaline plus FR139317 than in those receiving monocrotaline alone. CONCLUSIONS: These data suggest that blocking the action of endothelin-1 with a receptor antagonist ameliorates cardiac hypertrophy in this model system, and that this action is not mediated by ameliorating hemodynamic changes.

Follow-up of 2,733 Japanese patients with myocardial infarction.

Two thousand, seven hundred and thirty-three patients with acute myocardial infarction (AMI) who were admitted to our 11 institutions between 1983 and 1988, examined by coronary arteriography and discharged alive, were followed for an average of 2.9 years. During the follow-up period, 212 patients (7.6%) died. The factors that governed the prognosis of myocardial infarction after discharge were advanced age, female gender, obesity, previous infarction, angina pectoris more than 1 month before the onset of AMI, post-infarction angina, multiple-vessel diseases, advanced stage by Killip's and/or Forrester's classification on admission, elevated pulmonary capillary arterial pressure, decreased cardiac index, decreased left ventricular ejection fraction, increased left ventricular end-diastolic volume and left ventricular aneurysm before hospital discharge. Patients with ventricular tachycardia or ventricular fibrillation during hospitalization showed a poor prognosis. In contrast, patients who received intracoronary thrombolysis, or emergent and/or elective percutaneous transluminal coronary angioplasty showed a favorable prognosis.

Factors governing re-infarction in patients with myocardial infarction in Japan.

The subjects consisted of 2,733 patients with acute myocardial infarction (AMI) who were admitted to our 11 institutions between 1983 and 1988, examined by coronary arteriography, and discharged alive. The patients were followed for an average of 2.9 years after discharge. During the follow-up period, re-infarction occurred in 172 patients (6.3%). The factors associated with re-infarction were total cholesterol of more than 250 mg/dl, HDL-cholesterol of less than 35 mg/dl and diabetes mellitus. The rate of re-infarction was also high in patients who had had a previous infarction before admission, angina pectoris before or after the onset of AMI or multiple-vessel disease. In contrast, intracoronary thrombolysis reduced the rate of re-infarction.

Improvement of regional wall motion in medically treated myocardial infarction with single-vessel coronary artery disease.

Long-term changes in regional wall motion (RWM) following acute myocardial infarction (AMI) in 42 patients with uncomplicated single-vessel disease were examined retrospectively by repeat cardiac catheterizations. The first and second cardiac catheterizations were performed at an average of 28 days and 6.6 years after the onset of AMI, respectively. All 42 patients underwent first and second cardiac catheterizations without undergoing coronary artery bypass surgery or coronary angioplasty. Regional left ventricular functions were analyzed by the centerline method using a right anterior oblique left ventriculogram. The wall motion abnormality score (WMAS) was defined as [# chord below -2SD] x [mean SD chord below -2SD]. The improvement in the WMAS was more prominent in cases with an occluded infarct-related artery. Thus, we concluded that 1) RWM improves significantly with medical treatment in long-term follow-up in cases of uncomplicated AMI with single-vessel disease, and 2) the improvement of RWM is completed within the first few weeks after AMI in cases with a patent infarct-related artery.

Long-term prognosis of medically treated patients with acute myocardial infarction and one-vessel coronary artery disease.

Long-term prognosis was studied in 156 patients with acute myocardial infarction (AMI) with 1-vessel coronary artery disease (CAD). During a mean follow-up period of 110 months, 19 patients (14%) had reinfarction, 15 (9.6%) died (including 7 deaths of cardiac origin) and 15 (9.6%) were hospitalized for worsening of angina. A coronary arteriogram was obtained twice in 54 patients. The coronary arteriogram revealed multivessel CAD in all cases with reinfarction (n = 14). Ten percent of the patients with multivessel disease experienced a reinfarction during the initial 3 years after the onset of the first AMI. The recurrence rate of AMI in patients with 1-vessel disease increased gradually from the third year after the onset of their first AMI, reaching 10% in 6.7 years. The recurrence of AMI at the same region as the original infarction was detected in only 1 patient. Six of 19 patients (32%) with recurrence of AMI died and 13 survived after the reinfarction. It was difficult to predict future progression from the outcome of the comparison between the first and second coronary arteriograms. Thus, in patients with uncomplicated AMI with 1-vessel CAD, the prognosis is relatively good and the frequency of reinfarction is very low with conservative treatment.

[The acute and chronic effects of bunazosin on exercise capacity estimated by the anaerobic threshold in patients with chronic congestive heart failure].

To study the effect of bunazosin on exercise capacity in patients with congestive heart failure (NYHA II-III), anaerobic thresholds (AT, VO2, ml/min/kg) were measured before (control) and after initial 1 = 2mg administration of bunazosin (acute phase; N = 14) and after two weeks of bunazosin therapy (3mg/day, 1mg t. i. d., chronic phase; N = 6). AT were determined by Wasserman's V-slope method during ergometer exercise test with a ramp loading (10 watt/min). AT increased significantly from control during both acute (14.2 +/- 2.7 to 16.9 +/- 3.6 ml/min/kg p < 0.005) and chronic (13.6 +/- 2.5 to 16.7 +/- 1.0 p < 0.05) phase. Additionally, work (watt) attained at AT increased significantly from control during both acute (33.6 +/- 19.2 to 52.6 +/- 30.2 p < 0.005) and chronic (35.8 +/- 25 to 49.3 +/- 15 p < 0.05) phase. Pressure-rate-products (PRP, x 10(2) mmHg/min) at AT increased significantly from control during the acute phase (119 +/- 35 to 240 +/- 50 p < 0.005) alone. In the chronic phase, PRP decreased significantly at the work level equal to AT during control (from 207 +/- 41 to 187 +/- 39 p < 0.05). These data suggest that bunazosin has favorable acute and chronic effects on exercise capacity in patients with congestive heart failure.

Accelerated purine nucleotide degradation by anaerobic but not by aerobic ergometer muscle exercise.

The exact conditions under which exercise causes purine nucleotide degradation are not well understood. We determined plasma hypoxanthine and uric acid levels serially in eight individuals during ergometer muscle exercise. When the load was increased gradually by 15 W/min, plasma hypoxanthine was elevated only after the status exceeded the anaerobic threshold (AT), as determined by analysis of expired gas. Nonstrenuous ergometer exercise, which kept the status continuously below the AT, induced neither blood lactic acid nor plasma hypoxanthine elevation. These results suggest that the AT is also the threshold for the acceleration of purine nucleotide degradation. Muscle exercise to a degree that does not exceed the AT does not cause major purine nucleotide degradation, and, therefore, is expected to be beneficial for patients with gout and/or hyperuricemia.

[Antiplatelet therapy in cardiac diseases].

1) Myocardial infarction (MI): Aspirin (160-300 mg/day) therapy started immediately after the onset, with or without simultaneous coronary arterial thrombolytic therapy, reduces the mortality rate in vascular diseases, including MI, and prevents reinfarction. Maintenance therapy with the same dosage is also recommended. 2) Angina pectoris: In unstable angina, aspirin in a dose of 300 mg/day for 2 years reduces the mortality and the incidence of MI. Ticlopidine decreases anginal attacks in a few cases of angina at rest. 3) Coronary artery bypass grafting (CABG): Long-term administration of 325 mg aspirin/day should be started on the day of surgery and combined with 200-400 mg dipyridamole/day administered from 2 days before to 1 week after the surgery. 4) Percutaneous transluminal coronary angioplasty (PTCA): Current antiplatelet drugs prevent post-procedural acute coronary occlusion but not late restenosis.

Induction of diabetes by PolyI:C and anti-RT6.1 antibody treatment in DR-BB rats.

To determine whether environmental factors could affect the incidence of diabetes in RT6.1+ lymphocytes-depleted diabetes resistant (DR) BB rats, we tested polyinosinic-polycytidylic acid (Poly I:C), as an immune activator, in conjunction with anti-RT6.1 antibody in DR-BB rats which were bred in a specific pathogen free (SPF) condition. Diabetes was induced by the combined administration of poly I:C and anti-RT6.1 antibody. The use of poly I:C or anti-RT6.1 antibody alone did not cause diabetes. These results suggest that RT6.1+ T lymphocytes regulate autoimmune diabetes and that non-specific immune activation caused by environmental factors plays a key role in inducing diabetes in DR-BB rats.

Acute aortic dissection. A comparison between the results of medical and surgical treatments.

Over the last ten years 96 patients with aortic dissection were encountered in our Institute, of whom 51 had type A dissection, and 45 had type B dissection. In the patients with type A dissection the long-term survival rate was poor if they were not operated upon without delay, and the cause of death was usually rupture of the aneurysms. In the patients with acute type B dissection the surgical indication was limited and, generally speaking the long-term survival rate of the medically treated patients was more favorable.