Biomedical subjects

L Ceremuzyński

Publications and source records attributed to L Ceremuzyński.

At least 19 recordsLinked to original sources

PubMed2001

QT interval dispersion in ventricular beats: a noninvasive marker of susceptibility to sustained ventricular arrhythmias.

Increased QT dispersion (QTd) calculated from sinus beats has been shown to identify patients prone to sustained VT. However, predictive accuracy of this parameter is limited. Electrophysiological properties of the myocardium may be altered by a premature ventricular beats, which is a well-established trigger for sustained VT. Therefore, the author hypothesised that QTd in spontaneous or paced ventricular beats may improve identification of patients with inducible sustained VT. In 28 consecutive patients (men, mean age 61 +/- 13 years) who underwent programmed ventricular stimulation, the values of QTd calculated in sinus and ventricular beats were compared between inducible and noninducible patients. The mean QTd values obtained using three different methods differed significantly, QTd in paced ventricular beats being the highest, QTd in spontaneous ventricular beats was intermediate, and QTd in sinus beats was the lowest (83.9 +/- 30 vs 63.0 +/- 29 ms vs 53.9 +/- 27 ms, P < 0.0001 and P < 0.004, respectively). In 13 (46%) patients sustained VT was induced. QTd values were significantly higher in inducible than noninducible patients (QTd sinus beats: 67.5 +/- 31 vs 42.1 +/- 11 ms, P = 0.02; QTd spontaneous ventricular beats: 79.3 +/- 35 vs 46.7 +/- 13 ms, P = 0.008, and QTd-paced ventricular beats: 104.8 +/- 32 vs 65.9 +/- 9 ms, P = 0.0009). The receiver operator characteristic curves showed that at a sensitivity level of 100%, the highest specificity for identification of inducible patients had QTd measured in paced ventricular beats (87%) followed by QTd in spontaneous ventricular beats (45%), and QTd in sinus beats (40%). In conclusion, (1) QTd in ventricular beats is greater than in sinus beats, and (2) QTd calculated from paced ventricular beats identifies patients with inducible sustained VT better than QTd measured during sinus rhythm.

Electrocardiography↗

PubMed2000

Susceptibility to neuromediated syncope after acute myocardial infarction.

BACKGROUND: Syncope after acute myocardial infarction (AMI) is a common clinical problem. It may be hypothesised that remodelling and neurohormonal changes following AMI may predispose to neuromediated syncope. DESIGN: To address this issue we prospectively evaluated the incidence of positive results of head-up tilt-table testing in 40 patients following AMI and 40 age and sex matched controls without a history of syncope. The mechanisms of tilt-induced changes in autonomic tone were assessed using spectral analysis of heart rate variability. The patients were followed-up for one year. RESULTS: Positive results of tilt-test occurred in 4 (10%) controls and 13 (33%) AMI patients (P = 0.01). No significant differences in sympathovagal interaction (assessed by a low frequency/high frequency ratio) were detected between the groups before tilting (2. 9 +/- 1.9 vs. 3.1 +/- 2.2; NS). However, dynamic changes of this parameter differed significantly during the first 5 symptomless minutes of the active phase of tilt-test. The ratio increased in the majority of controls (87%) and decreased in the majority of patients (62%) (P < 0.0001). During one year follow-up, syncope or presyncope occurred in 10 (25%) AMI patients but did not occur in any control subject (P < 0.001). The sensitivity, specificity and predictive accuracy of an early tilt-test after AMI for the prediction of syncope or presyncope was 70%, 80% and 78%, respectively. CONCLUSION: Patients after AMI are prone to neuromediated reactions. Sympathetic withdrawal seems to be the most likely mechanism of syncope. The role of tilt testing for identification of patients susceptible to syncope or presyncope after AMI needs further investigation.

Adrenergic beta-Antagonists↗

PubMed2000

Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation.

OBJECTIVE: To assess the role of electrolyte imbalance in cardiac arrhythmias associated with congestive heart failure. DESIGN: Serum magnesium and potassium levels, urine magnesium excretion and the incidence of ventricular arrhythmias were assessed throughout the study. The patients who displayed complex arrhythmias after the first week of hospital medication were randomized 2:1 to double-blind magnesium supplementation or placebo. SETTING: The study was carried out in one municipal hospital, providing primary care. SUBJECTS: A total of 588 consecutive patients were screened for eligibility (clinical heart failure >/=6 months; NYHA class II-IV; left ventricular ejection fraction </=40%; sinus rhythm; serum creatinine </=2 mg dL-1). A total of 78 patients entered and 68 patients completed the study. INTERVENTIONS: Intravenous administration of magnesium (magnesium sulphate 8 g in 250 mL of 5% glucose) or placebo (250 mL of 5% glucose) over 12 h. MAIN OUTCOME MEASURES: (i) Incidence of ventricular arrhythmias in patients with hypomagnesemia; (ii) effects of magnesium supplementation on ventricular arrhythmias. RESULTS: On admission, hypomagnesemia was found in 38% and excessive magnesium loss in 72% of patients. Serum magnesium levels were lower and urine magnesium excretion was greater in patients with complex ventricular arrhythmias, both on admission and after treatment for heart failure. Intravenous administration of magnesium caused a significant decrease in the number of ventricular ectopic beats (P < 0.0001), couplets (P < 0.003) and episodes of nonsustained ventricular tachycardia (P < 0.01). CONCLUSIONS: Hypomagnesemia, probably related to increased urine magnesium excretion, is an essential feature of heart failure associated with complex ventricular arrhythmias. These arrhythmias can be alleviated/abolished by magnesium supplementation.

Aged↗

PubMed2000

Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.

AIMS: Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues. METHODS AND RESULTS: The study group consisted of 18 patients (all males, mean age 75 +/- 14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5 mg.kg(-1) or 10 mg.kg(-1) of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, P<0.009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion. CONCLUSION: Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias.

Aged↗

PubMed2000

[Micronized fenofibrate, decreased triglyceride levels, total cholesterol and LDL fractions in serum].

Elevated serum level of triglycerides is a classic indication for fibrates. Micronized fenofibrate is hypolipemic drug with proven safety and efficacy in a view of triglycerides reduction, but according to few papers published so far on the subject is also effective in decreasing elevated total and LDL cholesterol. The aim of study was to confirm results obtained from these few previous studies. Forty seven persons with lipid disturbances (25 males and 22 females, age range 34-71 yrs. mean 48.0) entered the study. Thirty two patients had a history myocardial infarction and fifteen persons without clinical symptoms of heart diseases. All of them were treated with micronized fenofibrate 200 mg daily. Micronized fenofibrate decreased serum concentration of total cholesterol by 13.4% (p < 0.01), LDL cholesterol by 21.2% (p < 0.001) and triglycerides by 39.5% (p < 0.001) in whole group of patients. Most beneficial effects were obtained in persons with mixed hyperlipidemia: reduction of total cholesterol, triglycerides and LDL cholesterol serum levels was 22.4% (p < 0.01), 52.5% (p < 0.0001), 25.4% (p < 0.01), respectively. In individuals with hypercholesterolemia a reduction of total cholesterol by 11% (p < 0.05) and LDL cholesterol by 15.4% (p < 0.05) was observed. In the group with hypertriglyceridemia or mixed hyperlipidemia reduction of serum triglycerides concentration by 33.5% (p < 0.05) was achieved. No significant change in serum HDL cholesterol level in any group was observed. The treatment with micronized fenofibrate was well tolerated. Our study shows that this drug is safe and seems to be effective in some cases with increased serum total and LDL cholesterol level as well.

Adult↗

PubMed1999

Low-dose glucose-insulin-potassium is ineffective in acute myocardial infarction: results of a randomized multicenter Pol-GIK trial.

We aimed to assess the clinical efficacy of glucose-insulin-potassium (GIK) in acute myocardial infarction. Experimental data provided evidence of the beneficial effects of GIK on ischemic myocardium. The clinical trials, mostly uncontrolled and conducted mainly before the thrombolytic era, were inconclusive due to the small number of patients and discrepancies in protocols. In order to evaluate the efficacy of this intervention, we have performed a prospective multicenter randomized study. The study consisted of 954 patients with acute myocardial infarction (MI) randomized within 24 hours from the onset of symptoms to low-dose GIK (n = 494), which consisted of 1000 mL 10% dextrose, 32-20 U insulin, and 80 mEq K-, or to the control group (n = 460), which was given 1000 mL 0.89% sodium chloride, by intravenous 24-hour infusion at a rate of 42 mL/h. Cardiac mortality and the occurrence of cardiac events at 35 days did not differ between GIK and control-allocated patients (32 (6.5%) vs. 21 (4.6%), respectively; OR 1.45, 95% CI 0.79-2.68, P = 0.20; and 214 (43.3%) vs. 192 (41.7%), OR 1.07, 95% CI 0.82-1.38, P = 0.62). Total mortality at 35 days was significantly higher in the GIK than in the control group (44 (8.9%) vs. 22 (4.8%), respectively, OR 1.95, 95% CI 1.12-3.47, P = 0.01). The excess of non-cardiac deaths in the GIK group may have occurred by chance. Low-dose GIK treatment does not improve the survival and clinical course in acute MI.

Aged↗

PubMed1998

Effect of early captopril treatment on blood adrenaline levels in acute myocardial infarction (the substudy of ISIS-4). International Study of Infarct Survival-4.

Of patients with acute myocardial infarction eligible for the International Study of Infarct Survival-4, randomized to captopril (n = 30) or placebo (n = 33), the captopril group had a significant decrease in blood adrenaline on day 3 compared with baseline values. Results suggest that suppression of sympathetic activity contributes to the beneficial effects of treatment with angiotensin-converting enzyme inhibitors in the early phase of acute myocardial infarction.

Aldosterone↗

PubMed1997

Effect of supplemental oral L-arginine on exercise capacity in patients with stable angina pectoris.

A randomized, double-blind, placebo-controlled study in patients with clinical symptoms of stable angina pectoris and healed myocardial infarction (n = 22) has shown that oral supplementation with L-arginine (6 g/day for 3 days) increases exercise capacity (tested on a Marquette case 12 treadmill according to the modified Bruce protocol). Results suggest that the inefficient L-arginine/nitric oxide system contributes to limitation of myocardial perfusion and/or peripheral vasodilation during maximum exercise in patients with stable angina pectoris.

Adult↗

PubMed1997

Clinical symptoms of mitral valve prolapse are related to hypomagnesemia and attenuated by magnesium supplementation.

Mitral valve prolapse syndrome (MVP) is a frequent disorder characterized by a number of complaints which lessen the quality of life. The pathogenesis of MVP symptoms has not been fully elucidated. Hyperadrenergic activity and magnesium deficiency have been suggested. This study was designed to verify the concept that heavily symptomatic MVP is accompanied by hypomagnesemia and to elucidate whether magnesium supplementation alleviates the symptoms and influences adrenergic activity. We assessed serum magnesium in 141 subjects with heavily symptomatic primary MVP and in 40 healthy controls. Decreased serum magnesium was found in 60% of patients and in 5% of controls (p <0.0001). Patients with low serum magnesium were subjected to magnesium or placebo supplementation in a double-blind, crossover fashion. Typical symptoms of MVP (n = 13), intensity of anxiety, and daily excretion of catecholamines were determined. After 5 weeks, the mean number of symptoms per patient decreased from 10.4 +/- 2.1 to 5.6 +/- 2.5 (p <0.0001), and a significant reduction in weakness, chest pain, dyspnea, palpitations, and anxiety was observed. Increased noradrenaline excretion before and after magnesium was seen in 63% and 17% of patients, respectively (p <0.01). Mean daily excretion of noradrenaline and adrenaline was significantly diminished after magnesium. It is concluded that many patients with heavily symptomatic MVP have low serum magnesium, and supplementation of this ion leads to improvement in most symptoms along with a decrease in catecholamine excretion.

Adolescent↗

PubMed1996

Effects of antioxidant vitamins C and E on signal-averaged electrocardiogram in acute myocardial infarction.

Experimental studies indicate that oxygen-free radicals contribute to ischemic myocardial damage and affect electric properties of cellular membranes. We hypothesize that an association exists between an oxygen-free radical-induced component of myocardial ischemic injury and altered electric function that underlies the genesis of ventricular late potentials in the course of myocardial infarction. If so, antioxidant vitamins C and E may prevent alterations in the signal-averaged electrocardiogram (SAECG). To test this hypothesis, we investigated the effect of supplementation with vitamins C and E on the indices of the SAECG in patients with acute myocardial infarction (AMI). Sixty-one patients with AMI were randomized to receive conventional treatment and vitamins C and E, each 600 mg/day, orally for 14 days (supplemented group, n = 33) or conventional treatment only (control group, n = 28). SAECG was recorded on days 1 or 2 and between days 9 and 13 (mean 10). Serum ascorbic acid, tocopherol, plasma lipid peroxides, and oxygen-free radical production by isolated leukocytes were measured on days 1 or 2 and between days 12 and 14. In the control group, SAECG showed an increase in mean QRS and low-amplitude ( < 40 microV) signal durations, from 99 +/- 10 to 111 +/- 13 ms (p < 0.001) and from 31 +/- 8 to 38 +/- 10 ms (p < 0.001), respectively, and a decrease in the root-mean-square voltage of the last 40 ms of the QRS complex, from 36 +/- 25 to 21 +/- 11 microV (p < 0.002). In vitamin-supplemented patients, all these indices remained unchanged. Oxygen-free radical production by isolated leukocytes was decreased compared with that in controls (p < 0.02). Supplementation was confirmed by elevation of serum ascorbic acid and tocopherol. Results support the hypothesis that in patients with AMI, oxygen-free radical-induced cellular damage contributes to alterations in electric function of the heart as seen on the SAECG.

Adult↗

PubMed1996

Intravenous amiodarone is safe and seems to be effective in termination of paroxysmal supraventricular tachyarrhythmias.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) and paroxysmal supraventricular tachycardia (PSVT) leading to hemodynamic compromise are among the most common reasons for admission to the coronary care unit (CCU) and need prompt and efficient therapy. Direct current cardioversion is the therapy of choice, but if found contraindicated or unavailable some antiarrhythmic agents are usually given to restore sinus rhythm. Many of these drugs have obvious limitations, especially in patients with acute myocardial infarction and/or heart failure. HYPOTHESIS: The aim of the present study was to assess the safety and efficacy of intravenous amiodarone in the acute termination of PAF or PSVT refractory to other antiarrhythmic agents in a large group of patients consecutively admitted to our CCU. METHODS: In the present study, we evaluated the safety and efficacy of amiodarone given intravenously in 142 consecutive patients with PAF or PSVT lasting < 24 h. In 37% of patients no evidence of underlying heart disease which may have caused arrhythmias were defined. A median of two other antiarrhythmic agents given prior to the first amiodarone injection had been ineffective. RESULTS: Sinus rhythm was restored in 91 patients (64%) (65% in the PAF group and 61% in the PSVT group). The mean time to rhythm conversion was 5.5 +/- 6.1 h for patients with PAF and 1.2 +/- 1.2 h for patients with PSVT. The mean dose of amiodarone administered up to conversion was 340 +/- 220 mg for PAF and 220 +/- 105 mg for PSVT. Except for transient first-degree atrioventricular block in two patients, no adverse effects possibly related to amiodarone were observed (including proarrhythmia and incidence or aggravation of heart failure symptoms). CONCLUSION: Amiodarone given intravenously for acute termination of supraventricular tachyarrhythmias is completely safe and seems effective. The results of this study, which is the largest ever made, indicate a need of randomized, controlled trials for the ultimate assessment of the efficacy of amiodarone in this clinical setting.

Aged↗

PubMed1996

Effects of captopril on ventricular arrhythmias in the early and late phase of suspected acute myocardial infarction. Randomized, placebo-controlled substudy of ISIS-4.

The antiarrhythmic effect of oral captopril was studied during the early (day 3) and late (day 14) phase of acute myocardial infarction among 304 patients in a randomized placebo-controlled substudy of ISIS-4. Ventricular arrhythmias (ventricular ectopic beats per hour) occurred significantly less frequently among captopril-allocated patients than among those allocated placebo at day 3 (logarithmic scale: 0.48 +/- 0.8 captopril vs 0.84 +/- 1.3 placebo; P < 0.003) and at day 14 (0.51 +/- 1.0 vs 0.77 +/- 1.3; P < 0.05). The number of patients with frequent ventricular arrhythmias (more than 10 ventricular ectopic beats per hour) was also significantly lower among those allocated captopril at day 3 (7.3% vs 14.4%; P < 0.05) and at day 14 (7.3% vs 14.8%; P < 0.05). These results support the hypothesis that the activation of the renin-angiotensin-aldosterone and sympathetic system may underlie heart rhythm disturbances in acute myocardial infarction, and that early use of converting enzyme inhibitor therapy may ameliorate these disturbances.

Adult↗

PubMed1996

Lack of effect of amiodarone on survival after extensive infarction. Polish Amiodarone Trial.

BACKGROUND: The purpose of this study was to elucidate whether the reduction of mortality with amiodarone after myocardial infarction depended on ejection fraction. METHODS: The data from the Polish Amiodarone Trial were analysed retrospectively. Patients with acute myocardial infarction and contraindications to beta-blockers were randomized on days 5-7 after admission to receive amiodarone (n = 305) or placebo (n = 308). Short and long-term (46 months) mortality were analysed comparing the groups with impaired (ejection fraction < 40%) and preserved (ejection fraction > or = 40%) left ventricular function. A subset of patients (n = 523) with available echocardiograms were subjected to this analysis. RESULTS: Long-term and sudden cardiac mortality were significantly reduced with amiodarone in the group of patients with ejection fraction > or = 40% (amiodarone versus placebo, respectively: 9.1 versus 16.5%, P < 0.05; 3.4 versus 8.2, P < 0.05). No beneficial effect of amiodarone was observed in the group with low ejection fraction (cardiac and sudden cardiac mortality: amiodarone versus placebo, 20.8 versus 19.3% and 7.8 versus 5.7% respectively). One-year mortality also revealed a favourable trend only in amiodarone-allocated patients with ejection fraction > or = 40%. CONCLUSION: Amiodarone decreased long-term and sudden cardiac mortality after myocardial infarction only in patients with preserved left ventricular function. No benefit was observed in patients with decreased ejection fraction.

Amiodarone↗

PubMed1995

Exercise producing alterations in the signal-averaged electrocardiogram in patients after myocardial infarction.

Late potentials are considered to be a marker for regional slow conduction which might predispose to reentrant ventricular arrhythmias. Since these arrhythmias may be induced by ischaemia it may be speculated that exercise-induced myocardial ischaemia may trigger late potentials. Exercise testing was performed in 53 patients early after myocardial infarction and in 20 healthy controls. Typical 12 lead ECG and signal averaged ECG (SA-ECG) from 12 leads were recorded before and after exercise testing. Changes in filtered QRS (QRS) and low amplitude signal durations, and in the root mean square voltage of the last 40 ms of the QRS complex (RMS40) were analysed. Thirty patients developed ST changes, consistent with transient ischaemia, that persisted during the SA-ECG recording after exercise. There were significant differences between baseline SA-ECG and SA-ECG after exercise in patients with positive exercise tests (QRS, 102 +/- 15 ms vs 114 +/- 15 ms (P < 0.01). LAS, 36 +/- 12 ms vs 42 +/- 11 ms (P < 0.05), and RMS40, 29 +/- 14 microV vs 20 +/- 13 microV (P < 0.01). No differences were observed in SA-ECG parameters in either patients with negative exercise tests or in controls. During follow-up, four patients died suddenly; all four had positive exercise tests and in three of them late potentials were induced by exercise. We conclude, that in post-infarction patients with positive exercise tests SA-ECG parameters deteriorate after exercise. This suggests that exercise-induced ischaemia triggers development of late potentials.

Adolescent↗

PubMed1993

Increase of R-wave in pre-discharge ergometric test after myocardial infarction indicates advanced left ventricular injury, latent serious arrhythmias and worse prognosis.

Changes in R-wave amplitude during exercise tests performed soon after myocardial infarction (15-31 days, mean 22) were analyzed in 78 men in relation to left ventricular injury (determined by 2-D echocardiography), ventricular arrhythmias (24-h Holter monitoring) and survival after myocardial infarction. It has been found that in patients with mild left ventricular injury (n = 51, Heger index < or = 3) the sum of the R-wave amplitude in 15 precordial leads recorded immediately after exercise decreased by 3.7 +/- 10% in comparison with resting values. In the patients with major left ventricular injury (n = 26, Heger Index > 3) the sum of R-wave amplitude after exercise increased by 12.9 +/- 17.5% (P < 0.001). Positive linear correlation (r = 0.35, P < 0.01) was observed between the level of left ventricular wall motion disturbances and R-wave amplitude changes. In patients with normal or slightly disturbed cardiac rhythm (n = 42, Lown scale 0-2) the sum of the R-wave amplitude after exercise decreased by 5 +/- 18% as compared to resting values, whereas in the patients with complex arrhythmias (n = 23, Lown scale 3-5) the sum of R-wave amplitude increased amounting to 9.9 +/- 17% (P < 0.001). Out of 17 patients who died during 5-year follow up, 16 displayed an increase or no change of the sum of R-wave amplitude. The same kind of relations between R-wave amplitude changes and left ventricular injury or cardiac arrhythmias were noted in patients with anterior and inferior myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Secondary prevention after myocardial infarction with class III antiarrhythmic drugs.

First-year mortality after myocardial infarction (MI) is high, amounting to 15%. It has been well documented that ventricular arrhythmias late after MI constitute a risk factor for sudden cardiac death. Consequently, several authors undertook attempts to decrease post-MI mortality with antiarrhythmic drugs. Unfortunately, the class I drugs most widely used in clinical practice proved to be ineffective or they even increased the risk of death, as occurred in the Cardiac Arrhythmia Suppression Trial (CAST). So far, only beta blockers, although not particularly effective in controlling ventricular ectopic beats, have been found to decrease first-year mortality after MI by 26-36%. Class III drugs appear to be promising in this clinical setting. Early study with sotalol showed a positive, although statistically nonsignificant, trend toward decreasing mortality. In a more recent trial with amiodarone (Basel Antiarrhythmic Study of Infarct Survival [BASIS]) done in Switzerland, total mortality was reduced (p < 0.05). It should be stressed that the drug was administered at a low dosage level (200 mg/day) to 98 patients and did not cause serious side effects. Similarly encouraging results have been provided by the Polish Amiodarone Study. Amiodarone given to 305 patients at a low dose (200-400 mg/day) reduced first-year cardiac mortality by 42% (p < 0.05). No serious side effects were noticed. Several ongoing trials should further substantiate the impact of this regimen on mortality after MI.

Amiodarone↗

PubMed1993

Ventricular arrhythmias late after myocardial infarction are related to hypomagnesemia and magnesium loss: preliminary trial of corrective therapy.

It has been well established that in acute myocardial infarction (MI) many patients display low serum magnesium (Mg). This is associated with complex ventricular arrhythmias. The question arises whether predischarge arrhythmias occurring late after MI might also be related to Mg imbalance. In 118 patients subjected to heart rhythm 24 h Holter monitoring in the second or third week after MI, we investigated (1) the relationship between serum Mg, urinary Mg loss, and ventricular arrhythmias, and (2) the effect of Mg supplementation on heart rhythm disturbances. In patients with undisturbed rhythm or monomorphic ventricular ectopic beats (VEB) (Lown 0-2; n = 84), mean serum Mg level (mg% +/- SD) was 1.83 +/- 0.21, whereas in patients with multifocal VEB, pairs, or nonsustained ventricular tachycardia (VT) (Lown 3-4; n = 34) serum Mg was decreased to 1.68 +/- 0.27 (p < 0.01). Serum Mg normal range in our laboratory is 1.7-2.6 mg%. The lowest serum Mg reaching 1.55 +/- 0.27 was found in nonsustained VT (Lown 4 b) subgroup (n = 14). Urinary Mg loss measured in 81 patients was more pronounced in those with Lown 3-4 arrhythmias (n = 26) than with Lown 0-2 (n = 55). The daily values were 73 +/- 22 and 54.4 +/- 26 mg, respectively (p < 0.001). Thirteen patients with complex arrhythmias and low serum Mg received Mg supplementation (MgSO4, 8 g in 500 ml 5% glucose intravenously during 24 h). This resulted in restoration of almost undisturbed rhythm in 10 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1993

Platelet adhesion is related to heart rhythm disturbances in the acute phase of myocardial infarction.

This study examines the relationship between platelet adhesion, aggregation and the occurrence of heart rhythm disturbances in 43 consecutive patients (mean age 58) admitted to a coronary care unit with acute myocardial infarction. Blood for platelet studies was taken prior to institution of any medication and heart rhythm was monitored (Holter) for 24 h after admission. The control group consisted of 22 healthy subjects (mean age 55 yr). Platelet adhesion to collagen was measured in EDTA-platelet rich plasma by recording the changes in light transmission in an optical aggregometer. Platelet aggregation was measured by the Born method. Platelet adhesion was increased in the group of patients with acute myocardial infarction as compared to controls and was significantly higher in the patients with complex ventricular arrhythmias (Lown 3-4b, n = 18) than in the patients with stable rhythm. Platelet aggregation in the patients with acute myocardial infarction did not differ significantly from the controls and was not related to heart rhythm disturbances. The causal relationship of increased platelet adhesiveness to collagen and heart rhythm disturbances in acute myocardial infarction remains to be established.

Adult↗