Tilt test results in young and elderly patients with syncope of unknown origin.

The effects of aging on the results of prolonged drug-free tilt testing were studied in 175 consecutive patients with unexplained syncope divided into 3 groups: 59 patients < 40 years old; 57 patients between 40 and 60 years; and 59 patients > 60 years old. Tilt-induced vaso-vagal syncope occurred respectively in 17 (29%), 20 (35%), and 18 patients (31%) in the 3 age groups. Vasodepressor, mixed, and cardioinhibitory vaso-vagal syncope occurred similarly in the 3 groups; organic heart disease and systemic hypertension were more frequent in elderly patients without affecting the incidence of tilt-induced syncope. Blood pressure and heart rate variations during syncope were similar in the 3 age groups; in the first 20 minutes of tilt testing, before the appearance of the vaso-vagal reflex, elderly patients showed greater reduction in blood pressure and smaller increase in heart rate than younger patients. Our data indicate that increasing age determines a different blood pressure and heart rate behavior during tilt testing, but apparently does not influence the incidence of vaso-vagal syncope in patients with syncope of undetermined etiology. As the proportion of patients with a positive isoproterenol tilt test was reported to decline with age, our results suggest that the reduced incidence of syncope during isoproterenol tilt testing could be the expression of impaired autonomic response among elderly syncope patients.

Effect of high-dose furosemide in refractory congestive heart failure.

High-dose firosemide is considered effective in primary renal sodium retention but is not generally recommended in congestive heart failure. In order to evaluate efficacy and safety of high-dose furosemide (greater than 500 mg/day), the authors studied 20 patients (pts) resistant to therapy (including furosemide less than 500 mg/day) selected from 161 pts admitted for chronic heart failure. All refractory pts (15 men and 5 women, mean age sixty +/- 12 years) were in NYHA class IV and showed hyponatremia (130 +/- 5 mEq/L) and impaired renal function (BUN 31 +/- 14 mg/dL, serum creatinine 1.3 +/- 0.3 mg/dL and BUN/creatinine ratio 23 +/- 7). In addition to digitalis, dopamine, angiotensin-converting enzyme inhibitors, or vasodilators, IV high-dose furosemide (775 +/- 419 mg/day, 500-2000) was given for ten +/- five days under daily clinical and laboratory monitoring. Three pts died of low-output syndrome while 16 pts were upgraded to NYHA class III and 1 pt to class II; a mean weight reduction of 7.3 +/- 2.9 kg in ten + five days (0.80 +/- 0.4 kg/day) and a mean diuresis increase of 88 +/- 57% occurred. The maximal dose of furosemide did not correlate with serum creatinine but did correlate with BUN/creatinine ratio (r = 0.78, p less than .001). Pts were discharged on with chronic heart failure, and 43% in the subgroup in NYHA class IV with hyponatremia. High dose furosemide was effective for rapid removal of excess water and salt in "furosemide-resistant" congestive heart failure. The relationship between renal impairment and maximal furosemide doses seems to confirm the role of renal pharmacokinetics in the appearance of furosemide resistance.

Prognostic value of hyponatremia in patients with severe chronic heart failure.

In order to evaluate the incidence and the prognostic value of hyponatremia (hypoNa) in patients (pts) with severe chronic heart failure (SCHF), the authors studied 161 consecutive pts (113M, 48F ages sixty-seven +/- ten) with SCHF in NYHA class III-IV. The cause of SCHF was ischemic in 64 pts, hypertensive in 39, valvular in 14, alcohol-related in 3, and idiopathic in 41. Pretreatment hypoNa (less than 135 mmol/L) was found in 64/161 pts (40%) (Group I); Na+ was less than 125 in 10 pts, 125-130 in 19, and 131-135 mmol/L in 35; 42/64 pts (66%) of Group I were in NYHA class IV at admission. In the pts with pretreatment Na+ less than 125 mmol/L, hypoNa was persistent and refractory to high-dose furosemide (less than 500 mg/day) and water restriction. Cardiovascular mortality of Group I pts was 69% within twenty-four months (34 pts died of low-output syndrom and 10 suddenly). All pts with Na+ less than 130 mmol/L died within six months. The 20 pts who normalized Na+ are alive, and in NYHA class II-III (follow-up: twenty-six +/- fifteen, six to sixty months). Pts without hypoNa were 97/161 (Group II), and 58/97 (60%) are alive (follow-up: thirty +/- eighteen, five to fifty-eight months), whereas 39 pts died (27 suddenly, 9 of low-output syndrome, and 3 of extracardiac disease) within twenty-four months. The mortality rate of Group II was significantly lower (40% vs 69%, p less than 0.001) compared with Group I. The two groups were similar for age, sex, and cause and duration of SCHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Direct determination of distribution volume and disappearance rate of native creatine kinase in humans.

Distribution volume (DV) and disappearance rate (Kd) of native creatine kinase (CK), parameters needed for enzymatic estimation of infarct size, have not been characterized in humans. Values for these parameters have been determined in experimental models and extrapolated for use in humans. During hemodynamic monitoring, 100 to 150 ml of enzyme-rich plasma was collected from 10 patients with acute myocardial infarction, stored at -30 degrees C for a maximum of 6 days, and then rapidly reinfused back to the same patient after return of CK serum activity to baseline levels. After reinfusion, blood samples were obtained at 5- to 15-minute intervals for 2 hours and at 30- to 60-minute intervals for an additional 10 hours. In each specimen, total CK activity and MM-CK and MB-CK concentrations were determined by spectrophotometry and radioimmunoassay. Data were analyzed by either nonlinear least-squares approximation or the noncompartmental approach after baseline subtraction. Concentration of immunologically active molecules appeared to decline in parallel to enzymatic activity. In three patients a double exponential decay was demonstrated. All others exhibited single exponential decay, with a Kd of 0.0023 +/- 0.00057 (SD) min-1. DV averaged 3284 +/- 693 (SD) ml, 5% of body weight. There was no correlation between Kd estimated from terminal portions of CK time-activity curves following infarction and Kd calculated after reinfused plasma. It was concluded that a one-compartment model using values for Kd and a DV compatible with plasma volume is suitable for clinical application, and that true Kd cannot be determined from the terminal portion of CK time-activity curves after acute infarction.

[Long term electrophysiological study on patients with acute myocardial infarction and complete heart block. Is cardiac pacing always necessary? (author's transl)]. / Studio elettrofisiologico a distanza in pazienti con infarto miocardico acuto complicato da blocco atrioventricolare completo parossistico. E sempre indicata l'elettrostimolazione cardiaca permanente?

UNLABELLED: Of 335 consecutive patients (pts) admitted to the coronary care unit (CCU) for acute myocardial infarction (AMI), 34 (10%) evidenced complete heart block (HB). The overall inhospital mortality was 14% (47 pts) versus 39% of the HB group (13 pts). No previous conduction disturbances were documented in 58% of pts before appearance of complete HB. Complete HB was preceded in 52% of pts by first or second degree HB or bundle branch block. Of 21 pts with HB discharged from the hospital, 5 (23%) died between 5 and 24 months (mean 12): no patients had sudden death; 16 pts (76%) are still alive after 13 to 45 months (mean 30). His bundle electrophysiologic (HBE) study was performed in 10 pts of the HB group after 4 to 40 months: 4 pts with anterior versus 6 with inferior AMI. Conduction disturbances were no longer present in all but one pt who had H-V 60 msec. Ajmaline (50 + 50 mg iv) prolonged A-H over 130 msec in 4 pts; H-V was not significantly increased in 8 of the 10 pts, while in two pts was 100 msec. One pt in the acute phase and one pt 12 months later, required pacemaker (PM) implant (both had inferior MI). IN CONCLUSION: no sudden death was documented during the follow-up period. The late HBE study, before and after ajmaline, did not allow to recognize critical conduction abnormalities suggessting prophylactic PM implantation.

["Pericarditis epistenocardica" as as a marker of extensive myocardial infarction. Clinical, electrocardiographic and enzymatic study (author's transl)]. / La pericardite epistenocardica come indice di infarto miocardico esteso. Studio clinico, elettrocardiografico ed enzimatico.

Pericarditis may complicate the early phase of myocardial infarction (MI). It occurs when necrosis involves the epicardial surface. To verify if pericarditis may be regarded as a marker of extensive MI, 60 patients with anterior or inferior MI admitted to the Coronary Care Unit within 6 hours from onset of symptoms, were studied by clinical, electrocardiographic and enzymatic parameters. 20 patients developed left ventricular failure (LVF) assessed by clinical, radiologic and hemodynamic indexes (15 mmHg has been considered the upper normal value for mean wedge pulmonary pressure). 9 of the 11 patients with pericarditis (PP) had LVF, versus 11 of the 49 non PP group (P = 0.002). Life threatening arrhythmias (ventricular tachicardia and fibrillation) appeared in 5 of the 11 PP versus 7 of the 49 non PP group (P = 0.04). No significant difference has been found between the two groups concerning the inhospital mortality. In a follow-up of 3 to 18 months, no difference in mortality was observed, while the functional recovery in the PP group was significantly worse (I and II versus III and IV New York Heart Association classes P = 0.003). Higher sigmaST values were found in precordial maps of the PP group, on admission (P = 0.03). After a deep spontaneous fall, sigmaST showed a reelevation which was similar in the two groups. SigmaR showed a greater % decrease however not statistically significant in PP. Creatinekinase enzymatic infarct size was significantly higher in PP group (P = 0.0002). It is concluded that pericarditis is a clinical marker of extensive MI and may be useful in evaluating prognosis and effectiveness of therapeutic interventions in MI.

[CK MB versus total CK in the estimation of myocardial necrosis. Comparative kinetic analysis and evaluation of an immunological method]. / CK MB verso CK totale nella quantificazione della necrosi miocardica. Analisi cinetica comparativa e valutazione di un methodo immunologico.

It has been suggested that the adoption of a relatively specific marker of the myocardial cell, such as creatine kinase MB isoenzyme, can yield improved accuracy in estimating infarct size by serial serum sampling and compartmental analysis. Nevertheless, current methods for the evaluation of isoenzyme activity are cumbersome and unsuitable for clinical use. We have therefore employed a new test for the rapid determination of CK MB activity, based on the immunological inhibition of M subunities. In 19 patients not submitted either to intramuscular injection or to repeated defibrillations, a good correlation was found between indexes of necrosis based on MB and total CK determination (r = 0.94), with the cumulative MB release amounting to 16 +/- 4% of total CK. Significant differences were observed in 3 patients submitted to external cardiac massage (MB = 9 +/- 1% of total CK) thus suggesting a considerable extracardiac source of total CK due to the trauma of the skeletal muscle. The comparative kinetic analysis shows substantial differences between the two isoenzymes, not only concerning the greater disappearance rate of CK MB but, more significantly, related to a faster release of this isoenzyme from the myocardium, which has not been previously reported. The good correlations found between maximal appearance rate and cumulative enzyme release (r = 0.86) suggest that the former may represent an index of the rate of degradation of cellular membranes. Practical implications of these data are discussed.

[Precordial mapping and enzymatic analysis for estimating infarct size in man. A comparative study (author's transl)]. / Mappaggio precordiale ed analisi enzimatica nella valutazione quantitativa della necrosi miocardica

To investigate the relationships between electrocardiographic and enzymatic indexes of infarct size (I.S.), a group of 19 patients with anterior infarction was studied by serial precordial mapping and CPK curves analysis. The time course of ST and QRS changes was examined and a sharp, spontaneous fall of sigmaST was shown to occur within 10-12 hours after onset of symptoms, followed by a gradual rise. sigmaST on admission appears to be a poor predictor of subsequent enzymatic I.S. (r=0.49). Good correlations with I.S. were observed, for sigmaST at 48-96 hours (r=0.82) and, especially, for the percent decrease of sigmaR, with respect to the initial values (deltaR%), (r=0.94).