Evolution of late potential parameters in thrombolyzed acute myocardial infarction might predict patency of the infarct-related artery.

The objective was to predict the patency grade of an infarct-related artery by identifying the time course of the changes of the late potential parameters before, during, and shortly after thrombolysis. The study population consisted of 51 patients with acute myocardial infarction (AMI) who received thrombolytic therapy within 3.2 +/- 1.3 hours from the onset of symptoms. Multiple signal-averaged electrocardiograms (SAECGs) were recorded before, during, and shortly after thrombolysis. A total of 489 single-averaged electrocardiographic tracings were evaluated. Late potentials were defined as: QRS duration > 114 ms, low amplitude signals (LASs) > 38 ms, and root mean square (RMS) < 20 microV. Late potentials were found in 37% of patients (21 before and 16 during the first 2 hours of thrombolysis), disappeared in all of patients within 89 +/- 75 minutes (range 25 to 350) but reappeared and persisted in 12% of patients, all with an occluded artery (grade 0). The late potential parameters (QRS, LAS, RMS) showed a gradual improvement which occurred earlier (2 vs 4 hours) and was more marked (0.01 vs 0.05) in cases with a patent artery. This improvement expressed by the late potential parameter index (LnQRS + LnLAS - LnRMS) predicts the patent artery with a sensitivity of 0.94 and specificity of 0.79. The improvement of late potential parameters jointly with close to normal initial values or the late potential parameter index and its changes constituted a satisfactory prediction of the patency grade. Thus, the signal-averaged electrocardiographic technique is capable of predicting the early success or failure of thrombolytic therapy.

Effect of protracted dobutamine infusion on survival of patients in cardiogenic shock treated with intraaortic balloon pumping.

UNLABELLED: The survival of subjects with postmyocardial infarction cardiogenic shock treated with intra-aortic balloon pumping (IABP) differs significantly among various reports. Differences in the criteria for IABP application and in the timing of its initiation have been considered as the main reasons for variations in survival. This study examines whether the way patients in cardiogenic shock are treated prior to IABP may affect their survival. Fifty-five patients in severe postmyocardial infarction cardiogenic shock were classified into three groups according to the rate of dobutamine infusion prior to IABP: the "nondobutamine" (group A, n = 31), the "high-dose dobutamine" (8 to 20 micrograms.kg-1.min-1, group B, n = 17), and the "low-dose dobutamine" (up to 7 micrograms.kg-1.min-1, group C, n = 7). All subjects seen from 1978 to 1983 were recruited for group A, from 1986 to 1990 for group B, and in years 1984, 1985, and 1991 for group C, without using any other classification criteria. It was shown a posteriori that the three groups did not differ in the features of the subjects, in the severity of shock, and in the time length between onset of shock and pumping initiation. None of the 17 subjects of group B could survive under pumping, while 10 of the 31 subjects in group A and 4 of the 7 subjects in group C were weaned off pumping. CONCLUSIONS: A protracted, high-dose pre-IABP administration of dobutamine may adversely affect the survival of patients with postmyocardial infarction cardiogenic shock.

Long-term intermittent dobutamine infusion combined with oral amiodarone improves the survival of patients with severe congestive heart failure.

STUDY OBJECTIVE: To evaluate the effects of long-term intermittent dobutamine infusion (IDI) with concomitant administration of low-dose amiodarone in patients with congestive heart failure (CHF) refractory to standard medical treatment. DESIGN: Prospective, interventional clinical trial. SETTING: Inpatient and outpatient heart failure clinic in a university teaching hospital. PATIENTS AND INTERVENTIONS: Twenty-two patients with CHF refractory to standard treatment who could be weaned from dobutamine therapy after an initial 72-h infusion were included in this study. The first 11 patients (group 1) were treated with IDI, 10 micromin, as needed (mean, once every 16 days, lasting for 12 to 48 h); the next 11 patients (group 2) received oral amiodarone, 400 mg/d, and IDI, 10 microg/kg/min, for 8 h every 7 days. MEASUREMENT AND RESULTS: There were no differences in baseline clinical, hemodynamic, and five biochemical characteristics between the two groups. The left ventricular ejection fraction was 13.5 +/- 4.5% in group 1 vs 15.5 +/- 4.9% in group 2 (mean +/- SD; p = 0.451); mean pulmonary capillary wedge pressure was 31.3 +/- 4.4 mm Hg vs 29.4 +/- 3.3 mm Hg (p = 0.316); serum creatinine was 1.9 +/- 0.4 mg/dL vs 1.6 +/- 0.5 mg/dL (p = 0.19); and serum Na was 139.6 +/- 6.2 mEq/L vs 138.4 +/- 3.1 mEq/L (p = 0.569). At 12 months of follow-up, 1 of 11 patients (9%) was alive in group 1 vs 6 of 11 patients (55%) in group 2 (p = 0.011). Furthermore, in group 2, the functional status improved significantly within the first 3 months of treatment, from New York Heart Association functional class IV to 2.63 +/- 0.5 (p = 0.0001). CONCLUSION: Long-term IDI in conjunction with amiodarone, added to conventional drugs, improved clinical status and survival of patients with severe CHF.

Autonomic control of the heart and peripheral vessels in human septic shock.

OBJECTIVE: Circulating endotoxin impairs the sympathetic regulation of the cardiovascular system in animals. We studied the changes in the autonomic control of the heart and circulation during septic shock in humans. DESIGN: 12 patients (age 43.0 +/- 6, 17-83 years) were investigated during septic shock (mean duration: 3.5 +/- 0.5 days) and during recovery, fluctuations in R-R interval, invasive arterial pressure (AP) and peripheral arteriolar circulation (PC, photoplethysmography) were evaluated by spectral analysis as a validated noninvasive measure of sympathovagal tone. Apache II score was adopted as the disease severity index. Low frequency components (0.03-0.15 Hz) of the frequency spectra were expressed as relative to the overall variability (LFnu) for each cardiovascular variable. RESULTS: LFnu were low or absent during shock but, in the 10 patients who recovered, increased by the time of discharge (post-shock). R-R LFnu increased from 17 +/- 6 to 47 +/- 9 (p < 0.03), AP LFnu from 6 +/- 3 to 35 +/- 4 (p < 0.02) and PC LFnu from 18 +/- 3 to 66 +/- 4 (p < 0.001). Apache II fell from 23.1 +/- 1, at admission, to 14.8 +/- 1.8 at discharge (p < 0.005). Two patients died showing no LFnu increase. CONCLUSION: Reduced LF components of the variability of cardiovascular signals are characteristic of septic shock, confirming the presence of abnormal autonomic control. Restored sympathetic (LF) modulation seems to be associated with a favourable prognosis.

Mechanical ventilation in conjunction with the intra-aortic balloon pump improves the outcome of patients in profound cardiogenic shock.

OBJECTIVE: To examine the effects of mechanical ventilation with positive end-expiratory pressure (PEEP), in conjunction with the intra-aortic balloon pump (IABP), on the outcome of patients in profound cardiogenic shock. PATIENTS: Twenty-eight consecutive patients presenting with myocardial infarction complicated by cardiogenic shock refractory to medical therapy, including dobutamine, dopamine and fluid administration. Eighteen patients were assisted by the IABP alone (IABP group), and ten patients by the IABP plus controlled mechanical ventilation with PEEP set at 10 cmH(2)O (IABP + CMV group). RESULTS: Weaning from mechanical assistance was accomplished in 8 out of 18 patients in the IABP group versus 9 out of 10 patients in the IABP + CMV group (p = 0.04). Ultimately, 5 of 18 patients in the IABP group were discharged from the hospital versus 8 of 10 patients in the IABP + CMV group (p = 0. 01). CONCLUSION: Mechanical ventilation with PEEP at 10 cmH(2)O supplements the IABP and may improve the survival rates of patients suffering from cardiogenic shock.

Myocardial salvage by the use of reperfusion and intraaortic balloon pump: experimental study.

BACKGROUND: Thrombolytic therapy improves left ventricular ejection fraction and survival. The study was undertaken to evaluate the effects of intraaortic balloon pump used in conjunction with reperfusion in reducing infarct size. METHODS: Twenty-two dogs were subjected to proximal left anterior descending coronary artery occlusion. In group 1 (n = 7) occlusion lasted for 6 hours. In group 2 (n = 6) 2 hours of occlusion was followed by reperfusion. In group 3 (n = 9) after 2 hours of occlusion the dogs were assisted with the intraaortic balloon pump throughout the 4 hours of reperfusion. At the end of 6 hours the infarcted myocardium of the left ventricle was determined and expressed as percentage of the myocardium at risk. RESULTS: In group 1, the infarcted myocardium was 79.3 +/- 9.9% of the myocardium at risk, in group 2, 59.0 +/- 19.9% (p < 0.05 versus group 1), and in group 3, 37.1 +/- 16.7% (p < 0.001 versus group 1 and p < 0.05 versus group 2). Endocardial viability ratio was increased by the intraaortic balloon pump; in group 1 it was 1.02 +/- 0.14, in group 2, 1.25 +/- 0.24, and in group 3, 1.47 +/- 0.31 (p < 0.001 versus group 1 and p < 0.02 versus group 2). CONCLUSIONS: Reperfusion and intraaortic balloon pump increased salvage of the ischemic myocardium over that achieved by reperfusion alone in a canine occlusion-reperfusion model.

Torsade des pointes and aprindine.

Aprindine was given orally to an 88-year-old patient with atrial fibrillation and ventricular premature depolarizations. The premature beats disappeared and sinus rhythm was restored on the third day of treatment. While on aprindine the QT interval was prolonged and the U wave became very prominent. The aprindine was stopped but 36 hr following the last oral dose, ventricular arrhythmia appeared with the characters of torsade des pointes. Three such episodes occurred within 24 hr. It is suggested that aprindine both eliminated the premature depolarizations and rendered the myocardium vulnerable by prolonging the QT interval. On discontinuing the medicament the premature beats reappeared while the myocardium was still vulnerable, so that torsade des pointes resulted.

Pressure-related ventricular tachycardia.

A case with syncope on exertion and paced heart block is presented. Non-sustained ventricular tachycardia was seen on Holter monitoring and reproduced repeatedly by either exercise or an injection of an alpha agonist, but not with provocative electrophysiology. Antihypertensive treatment using a beta-blocker with endogenous sympathomimetic activity prevented recurrences. It is suggested that this is a case of pressure-related tachycardia.

Atrial late potentials: paroxysmal supraventricular tachycardia versus paroxysmal atrial fibrillation.

The atrial signal averaged electrocardiogram has been used to detect patients at risk for paroxysmal atrial fibrillation but not yet for paroxysmal supraventricular tachycardia. The P-wave-triggered signal-averaged electrocardiogram, during sinus rhythm, was obtained from 97 subjects divided in groups as follows: 30 controls (Group C), 38 patients with documented paroxysmal atrial fibrillation (Group A) and 29 with documented paroxysmal supraventricular tachycardia (Group B). The atrial duration, root mean square of last 20 and 30 ms and the P-QRS segment were measured. Atrial late potentials were considered to exist when: atrial duration was > 120 ms and root mean square of last 20 ms were < 3.5 microV. The atrial duration (ms) was significantly shorter (P < 0.001) in Group C (113.4 +/- 8) than in Group A (138.5 +/- 23.8) and Group B (134.3 +/- 14.3). The root mean square (microV) of last 20 ms was significantly higher (P < 0.001) in Group C (5.2 +/- 2.5) than in Group A (2.5 +/- 1.3) and Group B (3.1 +/- 1.8). Atrial late potentials were present in 3/30 controls, 32/38 of Group A cases and 23/29 of Group B. The specificity and sensitivity were, respectively: 0.90, 0.84, for Group A, and 0.90, 0.79 for Group B. The P-QRS segment (ms) was significantly shorter (P < 0.01) in Group B (12.5 +/- 9.4) than in Group C (32.5 +/- 16.9) and Group A (20.5 +/- 13.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Limitation of infarct size by fixed coronary arterial stenosis maintained during reperfusion.

BACKGROUND: The effect on infarct size of a pre-infarction high-grade, fixed coronary arterial stenosis maintained during reperfusion, was evaluated. METHODS: This experimental study was carried out in the research laboratory of a University Hospital. A canine occlusion-reperfusion model was used. Twenty-eight dogs underwent proximal left anterior descending (LAD) coronary artery occlusion (O). In Group 1 (n=6) the O lasted for 6 hours. In Group 2 (n=6) the O lasted for 2 hours followed by 4 hours of reperfusion (R). In Group 3 (n=3), LAD was stenosed for 30 minutes followed by O for 6 hours. In Group 4 (n=7) LAD was stenosed for 30 minutes followed by O for 2 hours and then 4 hours of R during which the artery was kept stenosed at the same degree (fixed) as the initial one. In Group 5 (n=6) the protocol was identical to Group 4 with the additional use of the intra-aortic balloon pump during R. RESULTS: The infarcted myocardium was almost the same in Groups 1 and 3 (80.0+/-10.6% vs 77.3+/-3.8%, respectively, p=NS), but less in Group 2 (59.0+/-19.9%, p=0.046 vs Group 1). There were no hemodynamic differences between Groups 4 and 5 and the infarcted myocardium was almost identical in both groups (37.7+/-18.8% and 38.7+/-19.1%, respectively, p=NS). The combined results of Groups 4 and 5, regarding the infarcted myocardium, was 38.1+/-18% (p=0.037 vs Group 2). CONCLUSIONS: In this acute coronary occlusion model, a pre-existing high-grade stenosis that maintained during reperfusion increased the amount of salvaged ischemic myocardium.

Postpericardiotomy syndrome during intensive immunosuppression after cardiac transplantation.

A 15-year-old man with end-stage heart failure due to dilated cardiomyopathy, underwent heart transplantation. In the second postoperative week, while being treated with monoclonal antibodies (OKT3), cyclosporine and azathioprine, he developed a postpericardiotomy syndrome and cardiac tamponade, which necessitated emergency pericardiocentesis. Corticosteroids, administered according to the immunosuppression protocol, resulted in the prompt subsidence of the syndrome. This is the first report of a large pericardial effusion and cardiac tamponade due to a postpericardiotomy syndrome in an adult cardiac recipient.

Antihypertensive treatment for the management of premature ventricular complexes. Pilot study.

An acute increase in blood pressure (BP) may be associated with the appearance of premature ventricular complexes (PVC's) while an acute decrease in BP may reduce preexisting ones. Forty-two patients were studied in order to assess the critical BP value above which PVC's exist, the effect of chronic antihypertensive treatment on PVC's and the possibility to predict the antiarrhythmic effect of oral antihypertensive treatment by an acute test. Twenty-four subjects had over 10 min-1 PVC's at rest and received an intravenous sodium nitroprusside solution. Their systolic PB (SBP) was reduced from 156.3 +/- 34.1 (means +/- SD) mmHg to 96.2 +/- 21.3 mmHg and the PVC's from 29.6 +/- 10.7 min-1 to 4.5 +/- 9.0 min-1. The PVC's were completely eliminated in 16 cases and were fewer in the remaining 8 cases. When the SBP returned to its pre-test level, the PVC incidence also returned to its initial value. In 15 other cases with a SBP 134.9 +/- 18.3 mmHg and no PVC's at rest a metaraminol infusion was started. In 13 cases PVC's appeared at a SBP over 169.0 +/- 27.0 mmHg. The critical SBP below which there were no PVC's ranged widely in the 2 groups from below 75 mmHg to over 210 mmHg. In 11 cases of the nitroprusside group, 3 cases of the metaraminol group and 3 more cases a 24-hour Holter monitoring was applied. Then oral antihypertensive treatment was given (to 16/17 cases) for one week (amiloride 5 mg + hydrochlorothiazide 50 mg, supplemented, if needed, by methyldopa or hydralazine) and the Holter monitoring was repeated. The casual SBP measured before each Holter monitoring was initially 150.6 +/- 26.3 mmHg and was reduced by 20.3 +/- 15.4 mmHg (p less than 0.001). The number of 24-hour PVC's was 8469 +/- 10,007 and was significantly (p less than 0.005) reduced by 6077 +/- 7863 in all patients. The critical over casual SBP ratio was significantly (p less than 0.002) related to the 24-hour PVC's. It is concluded that the critical SBP varies widely in different persons and its determination by an acute BP-changing test may help in predicting to what extent an oral antihypertensive treatment may reduce the number of PVC's.

Diurnal variation of endothelial function and arterial stiffness in hypertension.

The onset of cardiovascular events presents a circadian variation that may be mediated by similar temporal patterns of vascular function. Blood pressure also follows circadian variation. We investigated the possible diurnal variation of endothelial function and arterial stiffness in patients with hypertension. Thirty-five individuals with recently diagnosed hypertension (mean age 48.3 years, range 30-60 years, 14 men) were examined. Flow-mediated vasodilatation (FMD), nitrate-mediated vasodilatation (NMD) and carotid-femoral (cf) pulse wave velocity (PWV) were measured at three different occasions: at 0700 hours immediately after awaking, at 1200 hours and at 2100 hours. FMD was markedly lower in the morning (0700 hours, 2.22+/-1.58%; 1200 hours, 4.37+/-2.25%; 2100 hours, 4.28+/-2.12%; P<0.001), whereas NMD was similar at the same time points. This difference remained significant after adjustment for baseline brachial artery diameter and reactive hyperaemia. PWVcf progressively increased from morning to evening (0700 hours, 9.8+/-1.9 m s(-1); 1200 hours, 10.2+/-2.2 m s(-1); 0900 hours, 10.5+/-1.9 m s(-1); P=0.013 for linear trend). Similar temporal patterns were observed in systolic and diastolic blood pressures peaking in the evening. PWVcf changes lost significance after adjustment for changes in mean blood pressure. Endothelial function is decreased in the early morning in hypertensive patients, whereas arterial stiffness is increased in the evening. Changes in BP-dependent passive artery distension may be involved in this phenomenon.

Spectral analysis of heart rate variability in the sepsis syndrome.

Sympathetic and parasympathetic activity was evaluated on 39 occasions in 17 patients with the sepsis syndrome, by measurement of the variation in resting heart rate using frequency spectrum analysis. Heart rate was recorded by electrocardiography and respiratory rate by impedance plethysmography. The sepsis syndrome was established on the basis of established clinical and physiological criteria. Subjects were studied, whenever possible, during the period of sepsis and during recovery. Spectral density of the beat-to-beat heart rate was measured within the low frequency band 0.04 to 0.10 Hz (low frequency power, LFP) modulated by sympathetic and parasympathetic activity, and within a 0.12 Hz band width at the respiratory frequency mode (respiratory frequency power, RFP) modulated by parasympathetic activity. Results were expressed as the total variability (total area beneath the power spectrum), as the spectral components normalized to the total power (LFPn, RFPn) or as the ratio of LFP/RFP. During the sepsis syndrome, total heart rate variability and the sympathetically mediated component, LFPn were significantly lower than during the following recovery phase (ANOVA, p < 0.0001, p < 0.01 respectively). Both APACHE II (Acute Physiological and Chronic Health Evaluation) and TISS (Therapeutic Intervention Scoring System) scores showed an inverse correlation with total heart rate variability, logLFP, LFPn and the LFP/RFP ratio (p < 0.002 to 0.0001). Sympathetically mediated heart rate variability was significantly lower during the sepsis syndrome and was inversely proportional to disease severity.

Acute changes in blood pressure as a cause of cardiac arrhythmias.

The effect of an acute change in blood pressure (BP) on ventricular ectopic activity and the influence of antiarrhythmic agents on this effect were examined in 24 patients. In 11 patients with premature ventricular complexes (PVCs), the BP was temporarily reduced by a sodium nitroprusside drip. In all of them the incidence of PVCs was reduced (or annihilated) by the induced hypotension. In 13 patients without ventricular ectopic activity, a metaraminol drip was given until either a PVC appeared or the systolic BP reached 200 mmHg, or symptoms appeared. In 12 cases at least one PVC appeared and in 8 of them the total number of PVCs was 13 or more, usually in the form of bigeminy. The repetition of the test following quinidine administration (serum quinidine level 1.7 +/- 0.5 ng ml-1) in 6 cases did not change this pattern, with one exception. It prevented the appearance of idioventricular accelerated rhythm in one case in whom this rhythm had been induced by the hypertension provocative test before the quinidine administration. All cases, in whom the test failed to induce more than 3 PVCs, had no cardiac problem at all. Six of the 8 cases in whom the test induced 13 or more PVCs had organic cardiac disease or palpitation. Other arrhythmias observed on BP elevation, were supraventricular extra beats, nodal escape rhythms and atrioventricular block. In one case with cardiomyopathy, the BP elevation was associated with early signs of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated with the generation of PVCs and its reduction with their reduction or disappearance.

Gout and neurological abnormalities associated with cardiomyopathy in a young man.

A 21 year old man with a family history of gout and neurological deficits, developed severe idiopathic congestive cardiomyopathy after a long history of typical gouty attacks and neurological abnormalities. Clinical and laboratory evaluations showed borderline mental retardation, ataxia, sensorineural deafness, marked hyperuricaemia, and excessive uric acid excretion in the presence of impaired renal function. None of the known causes of cardiomyopathy was found. Even though red cell hypoxanthine guanine phosphoribosyltransferase enzyme activity was normal, this case probably represents an inborn error of purine metabolism. The association of cardiomyopathy with gout is very unusual. Previously it has been only once described in a single case.

Clinical and laboratory parameters in adult diabetics with and without calcific shoulder periarthritis.

The clinical and laboratory parameters of calcific shoulder periarthritis (CSP) were examined in 900 patients with type II diabetes mellitus as well as in 350 age- and sex-matched control subjects. A threefold increased prevalence of CSP in diabetics compared with the control group was associated with the presence of longstanding and poorly controlled diabetes, hypercholesterolemia, and hypertriglyceridemia suggesting pronounced diabetic angiopathy, as well as with minor trauma and hypomagnesemia. Aging and serum calcium concentrations were not related to the presence of CSP. Thirty-two percent of diabetics with CSP were symptomatic; 15% of them presented with severe pain and restriction of shoulder movement. These findings confirm a close pathogenetic interrelation between CSP and diabetes mellitus.

Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study.

Two groups, one of 824 adult diabetics and one of 320 age and sex matched non-diabetics, were examined for abnormal glucose metabolism and calcifications on anteroposterior shoulder x rays. Two hundred and sixty two (31.8%) of the diabetics had shoulder calcification compared with 33 (10.3%) of the control group, with a preponderant localisation in the right shoulder. Diabetes of long duration treated with insulin for a long time was associated with a larger percentage of shoulder calcifications. These data and previous laboratory findings suggest a possible pathogenetic correlation between the prevalence of calcific shoulder tendinitis and diabetes.

Intravenous amiodarone decreases the duration of atrial fibrillation associated with acute myocardial infarction.

PURPOSE: Atrial fibrillation (AF) is a fairly common complication of acute myocardial infarction (AMI). The aim of this study was to examine the safety and efficacy of intravenous amiodarone in converting AF associated with AMI. METHODS: Seventy patients with AMI complicated with AF were prospectively divided into 3 groups: a) In group D (n = 26), 0.75 mg digoxin was administered intravenously and thereafter as needed, b) In group AM (n = 16), 300 mg of amiodarone was infused over 2 hours followed by 44 mg/hour for up to 60 hours or until sinus rhythm was restored, c) In group D + AM (n = 28), 0.75 mg of digoxin was administered (as in group D) for the initial 2 hours followed by amiodarone infusion as in group AM. RESULTS: Sinus rhythm was restored: a) by the end of the 2nd hour in 9/26 patients from group D, 4/16 from group AM, and 10/28 from group D + AM (p = NS), b) by the end of the 96th hour, in 18/26 patients from group D, and in all patients from group AM and groupd D + AM. The corresponding duration of AF was 51 +/- 34 hours, 17 +/- 15 hours and 9 +/- 13 hours, respectively (F = 15.4, p < 0.001). AF recurred in 9/26, 5/16 and 1/28 patients of groups D, AM and D + AM, respectively (p = 0.026). The required dosage of amiodarone was lower in the D + AM group than in the AM group (603 +/- 563 mg versus 1058 +/- 680 mg, p = 0.037). CONCLUSIONS: Intravenous amiodarone was well tolerated in patients with AMI complicated by AF and was effective in decreasing the duration of AF. However, the combination of amiodarone and digoxin was superior to amiodarone alone in restoring sinus rhythm faster, maintaining sinus rhythm longer, and allowing the use of a lower cumulative amount of amiodarone.