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Electrophysiological findings suggest that concealed anterograde conduction through accessory pathways may exist even during sinus rhythm in patients with so-called concealed Wolff-Parkinson-White (WPW) syndrome. To evaluate the pre-excitation characteristics in various types of WPW syndrome, high-resolution electrocardiograms were analyzed in 81 consecutive WPW syndrome patients and 50 age-matched normal subjects. The WPW group consisted of 30 cases of concealed WPW diagnosed by electrophysiological study, 38 cases of manifest WPW in which apparent delta waves were constant, and 13 cases of intermittent WPW in which the delta waves appeared periodically. The duration of the low-amplitude, high-frequency components of the signal-averaged filtered QRS complex that preceded the earliest upstroke of the surface QRS, including any delta waves (preceding potential duration, PPD), and the duration of low amplitude signals less than 10 microV (I-LAS10) or 20 microV (I-LAS20) were measured as parameters of pre-excitation. The PPDs in concealed and intermittent WPW were both significantly longer than in manifest WPW or in control subjects (6.8+/-2.7 ms, 7.9+/-3.5 ms vs 2.3+/-3.2 ms, 1.0+/-1.6 ms, both p<0.0001). Abnormally prolonged PPDs (>4 ms) were observed in 90% of concealed WPW cases and 76.9% of intermittent WPW, but in only 4% of normal subjects and 31.6% of manifest WPW. Both I-LAS10 and I-LAS20 in the 3 types of WPW syndrome were significantly longer than in normal subjects. The initial portion of the filtered QRS in concealed WPW closely resembled that of intermittent WPW. These results strongly suggest that in concealed WPW anterograde conduction through accessory pathways does occur and produces small amounts of pre-excitation even during sinus rhythm. The study concluded that, despite its name, concealed WPW is not completely concealed, and that non-invasive diagnosis during sinus rhythm is possible by using high-resolution electrocardiography to detect the concealed anterograde pre-excitation.

Based on the results of the Cardiac Arrhythmia Suppression Trial (CAST), strategies for the treatment of tachyarrhythmias have changed rapidly. The Japanese Antiarrhythmics Long-Term (JALT) study was planned to investigate the present methods for choosing antiarrhythmic drugs, and the effects on long-term prognosis in patients with tachyarrhythmias in Japan. Following a 6-month preliminary study (JALT-1), there was a multicenter nonrandomized prospective study (JALT-2), with a 2-year follow-up, of patients with paroxysmal atrial fibrillation (PAF), sustained ventricular tachycardia (SVT) and nonsustained VT (NSVT). Four hundred fifty-five patients were registered, and 361 of them (79%) were analyzed. Cerebral infarction occurred in 10 of 193 patients (5.2%) with PAF. Transition to chronic AF was observed in 21 patients (10.9%), but in none of the patients receiving Ca antagonist therapy. Twenty-five patients died: 5 deaths were arrhythmic, 10 were because of pump failure, and 9 were noncardiac. The most significant difference in drug selection between JALT-1 and JALT-2 was the increase in the use of slow kinetic Na channel blockers for PAF and the decrease in the use of the same agents for VT in the JALT-2 study. A marked change of therapeutic strategy occurred in JALT-2 compared with JALT-1. Most patients with a poor prognosis had underlying heart diseases and heart failure, but the per annum rate of death by arrhythmia and pump failure in JALT-2 was less than that in JALT-1.

The aim of this study was to elucidate the electrophysiologic characteristics and clinical significance of the accelerated junctional rhythm (JR) that remains after termination of radiofrequency (RF) current delivery during catheter ablation (CA) for atrioventricular nodal reentrant tachycardia (AVNRT). Fifty consecutive patients with AVNRT (21M, 29F, age 48 years) underwent RF-CA targeting the slow pathway. JR occurred at 124 out of a total of 236 ablation sites (53%) during the RF delivery. With 15 RF deliveries (6.4%, n=10), JR remained after termination of the RF delivery (Post-JR). The mean cycle length of the Post-JR immediately after termination of the RF delivery was 639+/-124 ms and its duration was widely distributed from 3 s to more than 1 h. The Post-JR exhibited a spontaneous rate deceleration and overdrive suppression by rapid atrial pacing. The JR during the RF delivery followed by Post-JR had a greater time span in which the JR appeared, compared with that without Post-JR. The Post-JR had less sensitivity(18 vs 96%), but greater specificity (97 vs 59%) and a positive predictive value (60 vs 39%) in predicting successful ablation compared with JR seen only during the RF delivery. It is concluded that the presence of Post-JR might be a reflection of the intense effect of RF energy on the nodal or peri-nodal tissue.

The aim of this study was to investigate the relationship between baroreflex sensitivity (BRS) and humoral factors in patients with congestive heart failure (CHF). BRS was assessed by the phenylephrine method in 16 patients with CHF and in 13 healthy controls. The CHF group was subdivided into 2 groups according to BRS (group A: <6 ms/mmHg, n=9; group B: > or =6 ms/mmHg, n=7). BRS was markedly depressed in CHF than in the controls (4.8+/-2.0 vs 8.3+/-3.6 ms/mmHg, p<0.01), and lower in group A than group B (3.3+/-1.3 vs 6.7+/-0.6 ms/mmHg, p<0.01). The plasma human atrial natriuretic peptide (h-ANP) level in group A was significantly higher than in group B (54.6+/-27.6 vs 18.0+/-7.4 pg/ml, p<0.01), and a significant inverse correlation was observed between plasma h-ANP and BRS (r=-0.635, p<0.01). However, there were no significant differences between the 2 groups in plasma catecholamine concentration, plasma renin activity and cardiac function by echocardiogram. These findings suggest that the elevation of endogenous ANP may also serve to compensate for impaired BRS in patients with CHF, in addition to its principal actions, such as diuresis and vasodilation.

This report describes a 49-year-old male with concealed Wolff-Parkinson-White syndrome in whom a true uncommon atrial flutter suddenly emerged 2 weeks after successful catheter ablation of a left-sided accessory pathway. The earliest atrial activation during the atrial flutter was recorded at the posterolateral mitral annulus 2 cm proximal to the previous successful ablation site for the accessory pathway. Two applications of radiofrequency (RF) current directed at the supravalvular mitral annulus could not terminate the atrial flutter. A subsequent delivery of RF current directed at the subvalvular annulus, where a local fragmented potential preceded the earliest atrial activation, eliminated the atrial flutter.

A case of Wolff-Parkinson-White (WPW) syndrome with several interesting electrophysiologic findings is presented. Although manifest preexcitation had not been documented in clinical routine check-ups for the 2 years before the ablation session, an intermittent preexcitation emerged after an initial unsuccessful radiofrequency current delivery directed at the subvalvular mitral annulus 1 cm distal from the subsequent successful ablation site. During intermittent manifestation of preexcitation, the following observations were made: (1) during manifest preexcitation, a possible Kent potential was recorded at the successful ablation site; (2) during non-preexcited impulse propagation, a local slow potential preceding the QRS complex (pre-QRS potential) was clearly observed at the same site; (3) the pre-QRS potential disappeared during orthodromic atrioventricular reciprocating tachycardia, spontaneous atrial premature contraction and after the subsequent successful ablation; and (4) when the pre-QRS potential was obvious, a small change in QRS morphology of the body-surface ECG was appreciable, compared with that during beats of negative pre-QRS potential. A comparable preceding component was also detected in a signal-averaged ECG. It is considered that the pre-QRS potential might be related to the anterograde concealed conduction through the accessory pathway.

The relationship between autonomic nervous system activity (ANA) and coronary vasoreactivity during transient myocardial ischemia was determined in patients with vasospastic angina (VA). ANA was measured by power spectral analysis of heart rate variability and humoral factors following intravenous infusion of insulin in 24 patients with VA and 6 control patients. Nine (38%) of the VA patients had significant ST segment depression (STD), and 4 of these patients had symptomatic STD. The frequency of anginal episodes in the 9 patients with VA and STD was significantly greater than that in the 15 VA patients without STD (3.4 +/- 3.1 vs 0.5 +/- 0.8 episodes/week, p < 0.05). The increase in the LF/HF ratio 30 min after insulin injection in patients with STD was significantly greater than that in patients without STD (34 +/- 31% vs 4 +/- 34%, p < 0.05). All of the patients with VA and STD had significant coronary vasospasm in response to the infusion of < or = 20 micrograms of acetylcholine, higher levels of nocturnal parasympathetic activity, and greater norepinephrine production in response to insulin stimulation than the VA patients without STD. These findings suggest that increased vagal tone and hyperreactivity to adrenergic stimulation may trigger vasospasm in patients with VA.

The incidence of purulent pericarditis has declined. However, mortality remains high. We describe a case of purulent pericarditis with tamponade caused by Salmonella enteritidis, and emphasize the importance of early recognition, prompt institution of appropriate antibiotic therapy, and early surgical drainage for survival.

The presence of mitral insufficiency after acute myocardial infarction (AMI) often leads to hemodynamic impairment and heart failure. This study was designed to examine the relationship between mitral regurgitation (MR), an indicator of mitral insufficiency, and the course of recovery from AMI. We evaluated the course of MR after AMI in 223 patients by color Doppler echocardiography. MR was detected in 21% (47/223) of patients at the onset of AMI, and developed in 18% (40/223) of patients during follow-up. Patients were grouped according to the course of MR as well as the success of acute recanalization therapy. No correlation was observed between the presence or course of MR and the site of infarction. The incidence of successful recanalization was higher in patients with MR that improved during follow-up than in patients with MR that was unchanged or that worsened during follow-up. Although no significant differences in hemodynamic variables were noted among the groups at admission, the group with unsuccessful recanalization and unimproved MR (BS-) showed a significantly greater left ventricular end-diastolic diameter (LVDd), left ventricular end-systolic diameter, and left ventricular end-diastolic volume (LVEDV) as well as a lower left ventricular ejection fraction than patients with successful recanalization and no MR (CS+) during the convalescent period. The extent of change in LVDd and LVEDV between admission and convalescence was significantly greater in the BS(-) group than in the CS(+) group. The results suggest that successful recanalization after AMI reduces the incidence of MR. Acute recanalization therapy after AMI may prevent left ventricular remodeling, resulting in a secondary improvement of MR.

Adenosine appears to mediate the preconditioning-induced reduction in infarct size in rabbits and dogs, but little is known about the role of adenosine in preconditioning-induced protection against ischemia-induced arrhythmias. We compared the effects of preconditioning induced by 2 cycles of 5 min of global ischemia and 2 cycles of 5 min of perfusion with either adenosine (100 mumol/L) or the adenosine A1-selective agonist 2-chloro-N6-cyclopentyladenosine (CCPA, 100 nmol/L) in protecting against ischemia-induced arrhythmias in Langendorff-perfused rat hearts. Preconditioning reduced the incidence of ventricular tachycardia (VT) from 100 to 58% and the incidence of sustained VT or ventricular fibrillation (VF) from 92 to 33%. Perfusion with adenosine reduced the incidence of VT from 100 to 55%, the incidence of VF from 67 to 9% and the incidence of sustained VT or VF from 92 to 9%. CCPA reduced the incidence of sustained VT or VF from 92 to 25%. These interventions provided a true reduction in the severity of arrhythmias, rather than merely a delay in the onset. Our results suggest that the stimulation of A1 receptor by adenosine is involved in triggering ischemic preconditioning-induced protection against ischemia-induced arrhythmias in rats.

The present study measured cardiac troponin T(TnT) for the pathophysiological analysis of evolving ischemic myocardial injury in 35 patients with unstable angina (3: Class IB, 32: Class IIIB) and in 40 patients undergoing coronary reperfusion therapy for acute myocardial infarction. Serum TnT, creatine kinase (CK), CKMB, myoglobin (Mb), and myosin light chain 1 (MLC1) were measured every 2-24 h for 10 days after admission to the CCU. In patients with unstable angina, positive test results were detected in 65.7% for TnT, 20% for CK, 37.1% for CKMB, 60.9% for Mb, and 26% for MLC1. Of the 23 patients with positive TnT, 12 (52.2%) had cardiac events. Of the 12 patients with negative TnT, 11 (91.6%) were event-free. All of the patients who developed cardiac events showed a persistent (n = 10) or delayed elevation (n = 2) pattern 28-120 h beforehand. The sensitivity for predicting cardiac events was 92.3% for TnT, 80% for Mb, 53.8% for CKMB, and 50% for MLC1. In patients with acute myocardial infarction, TnT release kinetics showed 2 peaks after coronary reperfusion therapy. TnT values at the 1st peak significantly correlated with maximum CKMB (r = 0.70, p < 0.05) and early-stage left ventricular wall motion score (r = 0.60, p < 0.05), while 2nd-peak TnT values significantly correlated with maximum MLC1 (r = 0.59, p < 0.05), the T1-SPECT score (r = 0.78, p < 0.05) and left ventricular ejection fraction (r = -0.74, p < 0.05) in the convalescent stage. The 2nd/1st-peak TnT ratio significantly correlated with the nQ/nST elevation index (ratio of the number of leads developing abnormal Q-wave 1 week after the onset to the number of leads showing ST elevation of more than 1 mm at admission) (r = 0.63, p < 0.05) in patients with anterior myocardial infarction. These data indicate that persistent release of TnT reflects progressive irreversible myocardial damage in unstable angina and indicates a risk of future cardiac events. In acute myocardial infarction, the 2nd/1st-peak TnT ratio in patients undergoing coronary reperfusion therapy may be useful for the quantitative evaluation of myocardial salvage.

Paroxysmal atrial flutter is a drug-resistant supraventricular tachyarrhythmia that is often accompanied by hemodynamic instability due to an excessive ventricular response. We report here a case of atrial flutter with 1:1 atrioventricular conduction, in which we were able to rescue the patient from a state of cardiogenic shock by using intravenous dofetilide, a new class III antiarrhythmic agent. Dofetilide was suitable for the treatment because it immediately increased atrioventricular nodal refractoriness without any negative inotropic action.

Myocardial bridge (MB) is a congenital anomaly of the coronary artery and may occur in 5 to 12% of the human population. However, the mechanism of MB-induced myocardial ischemia is still speculative. We report 2 cases of variant form angina pectoris associated with MB in which myocardial ischemia seemed to be related to the interaction between coronary perfusion and MB. In case 1, electrocardiography during anginal attack at rest showed ST elevation in the inferior leads and MB was observed after percutaneous transluminal coronary angioplasty at the site of the right coronary artery lesion following successful dilatation. In case 2, MB of the left anterior descending coronary was located in the identical portion where coronary vasospasm was induced by intracoronary acetylcholine injection, although ischemia during the spontaneous anginal attack was limited to the inferior area of myocardium. These 2 cases suggest that MB can be, at least in some patients, one of the possible causes of the endothelial damage which seems to be related to coronary vasospasm; this was documented in both cases.

The hemodynamic background associated with the occurrence of paroxysmal atrial fibrillation and flutter (PAF), in patient with acute myocardial infarction (AMI) were evaluated. Sixty-seven of 381 consecutive AMI patients (17.6%) were noted to have PAF in the acute phase of infarction. These 67 patients with PAF (group 1) were compared with 60 randomly selected patients without PAF (group 2). The hospital mortality rate was 25.4% in group 1, and 11.7% in group 2 (p less than 0.01). The hemodynamic variables measured before the onset of PAF in group 1, showed significantly more unfavorable values than those in group 2, which were measured at the time of admission. The 67 patients in group 1 were divided into 50 patients who survived (group S) and 17 patients who died in the hospital (group D). The hemodynamic status in group D demonstrated significantly larger deterioration before the onset of PAF than in group S. Hemodynamic variables were compared before and during PAF in groups D and S, cardiac index (CI) decreased significantly, and stroke index (SI) decreased by 46% in group D, with no decrease in CI and less decrease in SI (28. p less than 0.05) in group S. In conclusion, not only the occurrence of PAF, but the prognosis of patients with PAF is dependent on the severity of hemodynamic disturbance imposed by AMI. Atrial contribution to ventricular filling has great importance in the maintenance of the cardiac output in this patient population.

A study of the natural history of 51 adult patients with atrial septal defect with pulmonary hypertension (ASD + PH) was performed. ASD + PH of less than 14 Um2 of pulmonary artery resistance (PVR) was considered an indication for surgery. The prognosis of surgically treated patients was favorable, but that of medically treated patients was poor. For patients with ventricular septal defect with pulmonary hypertension (VSD + PH), surgery was considered for pulmonary-systemic vascular resistance ratio (Rp/Rs) less than 0.5, and for patients under than 10 years and, ideally, under 2 years of age.

To determine which therapeutic procedure is most appropriate for which type of aortic dissection, we investigated 146 cases of acute aortic dissection. In the group with dissection of the ascending aorta, 58.6% of patients given medical therapy and 48.8% of patients given surgical therapy died. In the group with dissection of the descending aorta, 14.0% given medical therapy and 50.0% given surgical therapy died. High mortality in the medical group with type A dissection was caused by delayed operation. Better survival was achieved in treated than surgically treated patients with acute distal dissection. In patients with cardiac tamponade, aortic regurgitation, hemothorax/hemo-mediastinum, visceral ischemia and peripheral ischemia, mortalities following medical treatment were fairly high. Surgical treatment brought on improvement in mortality in these groups. However, in the cases complicated by renal dysfunction, the mortality in the surgical group was higher than that in the medical group. 42 patients (28.8%) had no evidence of any complication and only 6 (14.3%) died. In 20 cases (47.6%) of uncomplicated dissection, no blood flow was observed in the false lumen. In cases with open false lumen, the following abnormal findings were more conspicuous: thrombocytopenia, decreased level of fibrinogen, increased fibrin degradation product and soluble fibrin monomer complex. However, these changes seem to be minimal in cases with thrombosed false lumen. The measurement of coagulation factors may be one useful method to determine which therapeutic procedure is most suitable.

Electron microscopic investigation was carried out to confirm our hypothesis, derived from a large number of macroscopic and light-microscopic observations, that impairment of the peripheral circulation of the myocardium, and not the presence of coronary thrombi, plays the fundamental role in the development of acute myocardial infarction. The peripheral coronary vessels of 5 human hearts obtained at autopsy showed severe histolytic impairment of the endothelial cells and of the tunica media muscle cells, even though no myocardial necrosis was observed either macroscopically or microscopically. An additional experimental study using 12 rabbits was performed to ascertain the induction of myocardial necrosis without coronary occlusion, by intravenous administration of either epinephrine or endotoxin alone or a combination of both. One-third of the epinephrine group and all of the combined treatment group developed myocardial necrosis. The intramyocardial vessels of these rabbits showed similar hystolytic changes to those observed in human cases. These findings support our concept that derangement of the peripheral circulation precedes the development of a coronary thrombus in cases of acute myocardial infarction.

Intracardiac stimulation (IS) has been widely used as the diagnostic method for various kinds of arrhythmias. Our results as to IS are as follows: 1) Since sinus recovery time (SNRT) closely correlated with basic cycle length (BCL) in 71 normal cases (r = 0.82, p less than 0.001), upper range of SNRT in normal was expressed as SNRT = 1.4BCL + 451 msec. 2) Paroxysmal supraventricular tachycardia (PSVT) induced by IS was fairly similar to the spontaneous PSVT (107 cases). Therefore, IS can be used to confirm the diagnosis of PSVT and also to evaluate the effectiveness of antiarrhythmic agents on PSVT. 3) Although induction or termination of ventricular tachycardia by IS may be useful in a general sense, dangerous tachyarrhythmias were sometimes provoked, indicating this test should be carried out under the utmost care.

Although subjective symptoms and brief recording of ECG have been used for an efficacy evaluation of new antiarrhythmics on ventricular premature contraction (VPC), incidence of subjective complaints in VPC was under 25% and number of VPC for 3 min did not correlate enough to those for 24 hours, indicating these parameters are not appropriate for such a trial. Number of VPC automatically counted by DECG (continuous ECG recording for 24 hours) showed high accuracy, while day to day variation of VPC arose as the next problem. While cases of more than about 7,000/day showed very little day to day variation, cases of less than about 1,000/day had poor reproducibility, indicating that the former group can be used for the trials of new antiarrhythmics, but not the latter group. For cases with medium magnitude of VPC variation, DECG should be recorded twice during the period without drug administration and application of the paired t-test for number of VPC in each corresponding hour may bring a good evaluation.

This study aims to clarify the neurohumoral regulation of cardiovascular circulatory adjustments and to analyze changes in renal function and their relationship to cardiovascular hemodynamics in the early stage of heart failure. Cardiac and peripheral (calf segment) hemodynamics, neurohumoral factors and renal function were investigated in totally 139 patients with acute myocardial infarction (AMI). Capacitance vessel constriction was observed in patients with uncomplicated AMI (Killip-I, Forrester HS-I) and constriction of capacitance and resistance vessels in patients complicated by heart failure (Killip II, Forrester HS-II) or cardiogenic shock (Killip III-IV, Forrester HS-IV). Augmented sympathoadrenal discharge significantly related to the degree of pump dysfunction (elevation of heart rate, central venous pressure, pulmonary capillary wedge pressure (PCWP) and decrease of stroke volume index (SVI] and activation of the renin-angiotensin-aldosterone system significantly related to fall in tissue perfusion pressure (mean blood pressure and calf vascular resistance) would be a possible mechanism for these compensatory mechanisms. However these would contribute to excessive vasoconstriction in limbs resulting in exercise intolerance or renal glomerular function impairment. The derangement of creatinine clearance, serum creatinine (Scr), blood urea nitrogen and beta 2-microglobulin were related to Killip classification, and it was clarified that PCWP tended to elevate more in patients with preexisting renal function disturbance, and when cardiac output (CO) depressed much lower, reduction of CO per se caused more severe prerenal renal insufficiency. That is, there were significant correlations between renal function parameters and cardiovascular hemodynamics. The Cardio-Renal Subset (CRS) was originally developed according to the initial SVI and Scr, and it was demonstrated that the CRS would be of definite predictive value in early identification of high risk patients.

A 22-year-old man with myotonic dystrophy associated with sick sinus syndrome is described. The patient showed marked weakness of grasping power, grip myotonia, percussion myotonia, bilateral cataracts, fixed facial expression and elevation of serum CPK level, and was diagnosed as having myotonic dystrophy. The Holter ECG showed marked sinus bradyarrhythmia at the rate of 25 beats per minute and the sinus node recovery time using overdrive suppression test was significantly prolonged. These findings indicated the patient also suffered from the sick sinus syndrome. Although various kinds of ECG abnormalities have been noted in the cases with myotonic dystrophy, there have been very few descriptions concerning the involvement of sinus node dysfunction in this disorder.

The early pre-hospital care of patients with acute myocardial infarction (AMI) is critical because of high mortality during acute phase of AMI. A CCU network has been established by the Metropolitan Tokyo CCU Communication Society and the help of the Ambulance Units through the Control Room of the Tokyo Fire Department, performing ECG telephone line transmission and telephone consultation. Out of 1439 patients admitted by means of CCU network during the 8-month period (Jan. 1982-Aug. 1982), 505 (30.3 percent) had AMI as a final cardiac diagnosis. Many patients were admitted directly to the CCU by ambulance from the place where the patient was located, with the shortest overall time of 7 hours 25 minutes. Fifty-three percent of patients with AMI were admitted within 6 hours after the onset of symptoms. The mean patients' decision time was 9 hours 48 minutes, which comprised one half of the overall period as well as physician delay of 6 hours 36 minutes on the average. Thus, community oriented educational programs to more fully inform the population and individual hospital evaluations to hospitalize patients with chest discomfort are needed in order to shorten the decision time and physician delay expediting the care of these patients.

Unlabelled: The effects of intraaortic balloon pumping (IABP) were studied in 91 patients with acute myocardial infarction complicated with cardiogenic shock (75 pts), ventricular septal perforation (VSP) (12 pts), and/or mitral regurgitation (MR) (4 pts). Out of 44 pts with cardiogenic shock in whom IABP was performed, 14 pts could not recover from cardiogenic shock, 6 pts became dependent on IABP and 13 pts survived (29.5%). In contrast, out of the remaining 31 pts with cardiogenic shock who did not undergo IABP because of inability to insert IABP catheter or other reasons and were treated medically, only 3 pts survived (9.7%, p less than 0.05). After the initiation of IABP, BPd, CI, SVI, SWI, TMG increased significantly, and HR, CVP, PCWP, TPR decreased significantly. Comparison of hemodynamic parameters after the initiation of IABP showed that SVI and SWI at 24 hours were higher and CVP lower in survivors. Out of 7 pts with VSP who underwent IABP 2 pts were operated and survived., In Conclusion: short-term mortality in pts with cardiogenic shock was significantly lower in IABP-treated group, hemodynamic parameters improved after IABP, survivors from cardiogenic shock had higher SVI, SWI, BPd, and lower CVP than non-survivors, patients with VSP and MR had worse prognosis in spite of IABP.

This study was performed to delineate the precise features and the treatment of ventricular tachycardia (VT) with acute myocardial infarction (AMI). Results indicate: 1) the incidence of VT in 310 AMI patients was 16.1% (50 patients); 2) the higher incidence of ventricular fibrillation and mortalities were observed in VT group compared with non-VT group; 3) the incidence of VT was higher in inferior infarction group (21.0%) than anterior group (13.1%); 4) more frequent VT were seen in patients with more severe heart failure; 5) two peaks of VT occurrence, on the first day and in the 4th week after the onset of AMI, were recognized especially in anterior infarction group; 6) supraventricular arrhythmias were more frequent than ventricular premature beats during one minute preceding VT; 7) the successful termination of VT was achieved in 63.9% of episodes by thump-version, 61.5% by lidocaine, 66.7% by disopyramide and 100% by mexiletine; 8) prophylactic effect on VT by class Ia antiarrhythmic agents seemed stronger than others; 9) IABP was effective to prevent VT in some cases; 10) poor prognosis was determined by frequent and later onset of VT, and combination of severe heart failure.

We studied the effects of positive end-expiratory pressure (PEEP) ventilation in ten patients with acute myocardial infarction (nine in Killip class III, one in Killip class IV; pulmonary capillary wedge pressure greater than 24 mmHg) and of extracorporeal ultrafiltration method (ECUM) in seven patients with refractory heart failure due to acute myocardial infarction and others. Application of PEEP resulted in significant increases in PaO2 and SaO2 and decrease in PaCO2. Significant reduction in mean pulmonary arterial and pulmonary capillary wedge pressures and heart rate was observed, while stroke work index increased significantly. There was a significant correlation between changes in stroke work index and PaO2 after the application of PEEP. The use of ECUM removed fluid of 1416 +/- 662 ml (680-2800 ml) with the ultrafiltration flux rate being 478 +/- 223 ml/hour. Significant decreases in mean pulmonary arterial, pulmonary capillary wedge and central venous pressures were observed, while PaO2 increased significantly. BUN and serum creatinine levels increased significantly, and total protein and serum albumin tended to increase. There was a significant correlation between fluid removed and change in PaO2 after the use of ECUM. Thus, PEEP and ECUM are beneficial for patients with refractory heart failure. The mechanism(s) are: reduction in preload due to an increased intrathoracic pressure and a decreased systemic venous return with PEEP, or due to removal of excess fluid with ECUM, and improvement of the oxygenation of the blood.

A retrospective analysis of 44 patients was carried out to evaluate the efficacy of class IA antiarrhythmic drugs (disopyramide and/or procainamide), and of drugs of one or more other classes by means of 24-hour Holter recording. This study included only patients who exhibited 5000 or more ventricular premature complexes (VPCs) during a 24-hour pretrial baseline recording. The drugs that reduced the frequency of VPCs by at least 50% were considered effective. Eighteen patients (41%) responded to class IA drugs (responders) and 26 patients (59%) did not (nonresponders). There was a significant difference between the two groups in relation to the types of disease (p less than 0.01), but no significant difference with regard to other clinical and electrocardiographic characteristics. There was a significant discordance between trials of class IA drugs and class IC drugs (p less than 0.05). The efficacy of class IA drugs is very similar to that of class IB drugs, and only class IC drugs represent the highest efficacy in patients refractory to both class IA and class IB drugs. In conclusion, when ventricular arrhythmias do not respond to class IA or IB drugs, class IC drugs could be chosen as the next regimen.

The purposes of this study were to investigate the sequential changes of PMN elastase during evolving myocardial infarction, and also to ascertain whether or not ulinastatin (UL), a clinically useful protease inhibitor, would affect the extent of ischemic myocardial injury. The levels of plasma PMN elastase (as alpha 1-proteinase inhibitor-elastase complex) were measured once in 13 normal controls, and at intervals in 30 acute myocardial infarction (AMI) patients given UL and 30 AMI controls on conventional therapy, and compared between the groups. The levels in control group on conventional therapy were significantly higher from 6 to 72 hours after the onset than those in normal controls. Maximum PMN elastase levels in non-survivors (n = 7) were significantly higher than in survivors (n = 23) at the 6-month follow-up (288.7 +/- 75.8 vs. 188.1 +/- 56.9 micrograms/l, p less than 0.01). The maximum level of PMN elastase in patients given UL was significantly lower than that in the control group (162.2 +/- 96.2 vs 207.3 +/- 70.1 micrograms/l, p less than 0.05), and the peak CK-MB in patients given UL was significantly lower than that in controls (252.3 +/- 150.9 vs 360.1 +/- 239.6 IU/l, p less than 0.05). Early mortality (seen at 6-month follow-up) in patients administered UL was significantly lower than that of the treated controls (3.3% vs 23.3%, p less than 0.05). Analysis of changes in PMN elastase levels suggested that UL would be clinically beneficial for reduction of ischemic myocardial injury.

Since it is still controversial as to whether or not atrial natriuretic peptide (ANP) antagonizes norepinephrine (NE)-induced vasoconstriction, we examined the interactions of ANP and NE with respect to renal circulation. (I) Although ANP infusion at 25 ng/kg/min for 40 min caused a decrease in total peripheral resistance (-11%, p less than 0.01) in 34 patients with cardiovascular disease and 15 normotensives (NTs), renal vascular resistance (RVR) was not reduced consistently by ANP. However, there was a negative correlation between changes in RVR and the preinfusion plasma NE level (r = -0.51, p less than 0.001). (II) When NE infusion into 6 NTs at 100 ng/kg/min was followed by ANP infusion, urinary Na excretion was increased to a greater degree than that by ANP infusion alone (+234% vs +34%, p less than 0.01). Furthermore, ANP brought about a recovery in NE-induced falls in renal blood flow (+40%) and glomerular filtration rate (+38%, both p less than 0.05). These effects were attributed to both a decrease in calculated renal afferent resistance and an increase in efferent resistance (-43% and +17%, respectively, p less than 0.05). Thus, increased sympathetic nervous activity seems to augment the renal effects of ANP, and the antagonistic effects of ANP to NE-induced preglomerular vasoconstriction may counteract Na retention caused by excessive sympathetic tone.