![Graphic][1] A 20 year old man, with a history of cocaine and amphetamine abuse, was admitted to the coronary care unit with mild exertional dyspnoea. His ECG and cardiac enzymes were normal. A transthoracic echocardiogram showed a … [1]: /embed/graphic-1.gif

BACKGROUND:Several studies have observed a circadian pattern in the onset of acute myocardial infarction (AMI), with a peak incidence in the morning hours. It has been suggested that different circadian rhythms may exist in various subgroups of patients.METHODS:This study sought to determine whether the circadian incidence of AMI varied by sex, age, cardiovascular risk factors, previous history of ischemic accidents, the site of AMI, and the short-term outcome. These possibilities were examined in a population of 597 consecutive patients with AMI, admitted to the coronary care unit. 548 patients have been included in the study, 442 men (80.6%) and 106 women (19.4 %); mean age 64.5 years.RESULTS:A peak incidence of AMI was found between 06.01 a.m. and 12.00 a.m. (32.4%; p<0.0002). This peak was present in patients 65 years old (33.2%; p<0.005), in men (32.5%; p<0.0002) but not in women, in smokers (32.1%; p<0.0005) and in those that did not smoke (33.0%; p<0.04), in patients with hypercholesterolemia (34.9%; p<0.006 ) and without hypercholesterolemia (31.1%; p<0.03). A circadian rhythm was absent in diabetics, hypertensives and in patients with a history of previous cardiovascular events. Regarding the site of AMI, inferior AMI showed an increased incidence between 06.01 a.m. and 12.00 a.m. (36.2%; p<0.002), while the circadian distribution of anterior AMI, as well as non-Q wave AMI, did not show this incidence. Finally, higher mortality was reported in patients with an AMI onset at night (22.3%).CONCLUSIONS:These results give further clues in understanding the external and inner factors acting in the morning hours as triggers for AMI.

BACKGROUND:This work aims to correlate retina vessel alteration with the possible presence of coronary alteration in the same patient.METHODS:For this purpose 103 patients have been studied. Of these, 63 had symptoms of coronary heart disease while the remaining 40 were used as a control. 29 patients, out of the 63, were also afflicted with angine while 34 had previously had myocardial infarction. Eye fundus tests and coronarography have been carried out, and risk factors such as high cholesterol, high blood pressure, diabetes and smoking have been investigated.RESULTS AND CONCLUSIONS:This work shows that there is a close correlation between a positive eye fundus and coronarography alteration whereas a negative one is not incompatible with organic lesions. A positive eye fundus due to alteration of retina microcirculation can be indicative of atherosclerosis in symptomatic patients.

The aim of this study was to investigate the circadian variability of heart rate in acute myocardial infarction (AMI) in identifying patients at high risk for malignant ventricular arrhythmias (MVA) and sudden death within 1 year of the acute event. The investigation was carried out in 43 patients, who underwent 24-hour Holter monitoring within 3 months of AMI. Besides the time domain indexes of heart rate variability (SDNN, SDNN index, pNN50, rMSSD), the circadian rhythm of hourly total beats (HTB) and hourly qualified beats (HQB) has been analyzed by the Cosinor method. The AMI patients with MVA and those with MVA who died within 1 year the acute event showed SDNN, SDNN index and pNN50 values lower than subjects without MVA and survived patients with MVA, respectively; the individuals with AMI at high risk for MVA and for sudden death had an SDNN value < 105 ms and 50 ms, respectively. The circadian rhythm of HTB and HQB was statistically validated only in the group without MVA; patients without the circadian rhythm of HTB and HQB showed a higher mortality rate within 1 year of AMI, and the majority was in the group with MVA. The contemporary evidence of an SDNN value < 105 ms and the lack of HTB and HQB circadian rhythm increased sensitivity for identifying patients with MVA to 75%. On the other hand, the contemporary evidence of an SDNN value < 50 ms and the lack of HTB and HQB circadian rhythm increased sensitivity for identifying patients who died within 1 year of AMI to 100%. In conclusion, the assayed methods seem to be both useful and complementary in identifying patients at high risk for MVA and sudden death within 1 year of AMI.

UNLABELLED:Cigarette smoking is commonly considered as a major risk factor for Acute Myocardial Infarction (AMI). Although AMI has a high incidence in smokers, it doesn't seem to correlate with a worse in hospital prognosis. In order to investigate if cigarette smoking does affect the in-hospital prognosis in patients with AMI, 590 consecutive patients (451 males and 139 females; mean age 63.4 years) admitted to the Coronary Care Unit (CCU) with definite AMI have been studied. Patients were divided in two groups: Group A (303 patients, 269 males and 34 females) smokers till AMI and Group B (287 patients, 182 males and 105 females) nonsmokers or smokers till a month before AMI. RESULTS:The mean age of nonsmokers was higher than smokers (68.4 years vs 58.8 years; p < 0.001). In addition they showed more frequently hypertension (48.8% vs 38%; p < 0.001), diabetes (31.3% vs 16.3%; p < 0.001), and healed infarction or angina (45.6% vs 37.5%). Among Group B higher global mortality rate was observed (22.6% vs 7.6%; p < 0.001) either among thrombolysed patients (10.1% vs 4.4%; p < 0.001) either among not thrombolysed (26.9% vs 4.4%; p < 0.001). The grading in age classes confirmed a higher mortality in nonsmokers patients (6.7% vs 4.9% age > or = 40 and < or = 65 years; 32.5% vs 13.3% > 65 years). They also presented more frequently arrhythmias (15.3% vs 12.2%), ischemic complications (25.4% vs 18.7%), and congestive heart failure (46% vs 34.2%). CONCLUSIONS:According to other authors the results of this study confirm a better prognosis in smokers with AMI. Up to authors hypothesis this outcome could be related either to the younger age, a to a different pathogenetic mechanism of coronaric occlusion to raised thrombosis.

In the last decade advances in cardiovascular research improved remarkably our understanding of coronary heart disease. However many important problems are so far unresolved. In the present study we focused on the "natural" history of ischemic heart disease in a group of 114 patients. One hundred-seven patients had recent myocardial infarction, and seven suffered from angina. They were observed for a mean period of five years (one to 168 months). Forty-nine patients (42.9%) had no coronary events; sixty-five had angina, myocardial infarction or both. The myocardial infarction was however rare (five cases). The most frequent presentation of angina was stable and effort angina, which sometimes subsided after a period of presence. The classification of angina was often very difficult in cases of effort angina with very low threshold. No relevant differences were found between patients with and without coronary events according to age, sex, duration of follow-up, location of previous myocardial infarction. A significant difference was found in the prevalence of risk factors only for hypertension, which was more frequent in patients with coronary events. Smokers were more frequent in group without coronary events. In our opinion, the most interesting conclusion is that, almost half of these patients remained completely asymptomatic for a very long period.

Two hundred and one patients admitted to Coronary Care Unit with documented acute myocardial infarction, whose chest pain had occurred within 12 hours of hospital admission non thrombolised, were studied. The peak of creatine kinase (CK) was examined and compared between patients without previous manifestations of myocardial ischemia (group A, 106 patients) and patients with/history angina pector or healed myocardial infarction (group B, 95 patients). The mean peak creatine kinase level in the negative history group was higher (2261 +/- 226 U/L vs 1779 +/- 97 U/L p < 0.001), especially in patients aged less than 65. No significant difference was observed in patients aged more than 64 of the two groups. Patients with a positive history presented more frequently ischemic complications (p < 0.05) while the frequency of hemodynamic disturbances and arrhythmias was not significantly different. Total mortality was similar in the two groups (22.6% vs 21%) and more frequently occurred in older patients with congestive heart failure. The authors form the hypothesis that the higher mean peak creatine level in patients without previous myocardial ischemia is the result of absence of coronary collateral circulation. The presence of collateral vessels permits less extensive myocardial infarction but it does not change the prognosis.

The incidence of hypotension in patients treated with thrombolytic agents for myocardial infarction was investigated in a series of 71 patients, 17 treated with urokinase, 35 with rtPA and 19 with APSAC. Hypotension was observed in 23.5% of the first group, in 5.5% of the second, and in 42.10% of the third (p < 0.002 between rtPA and APSAC). In the inferior location hypotensive reaction was much more frequent than in anterior one (p < 007) especially if a right ventricular involvement was associated. Even if hypotension is a minor and generally harmless complication, it poses many practical problems, and its occurrence must be taken into account when choosing a fibrinolytic treatment.

BACKGROUNDCarbamazepine (CBZ) is a first-line drug in the treatment of epileptic seizures and neuralgia. CBZ is also a cardioactive drug and sometimes induces sinusal dysfunction or AV conduction defects.METHODSIn order to investigate the effect of CBZ on sinus node function and AV conduction, long-term ECG recording (24 hours) and determination of plasma concentration of CBZ were carried out in 10 epileptic patients without heart disorders (5 males and 5 females, mean age 31 years), in the basal state, during steady-state (7th day) and after 30th day of CBZ treatment. The number of total cardiac beats, mean heart rate, P-Q and Q-T interval, sinus-atrial node and atrioventricular dysfunction and intraventricular conduction delay were evaluated.RESULTSPlasma CBZ concentration was always in the therapeutic range (5-12 micrograms/ml): 9.5 micrograms/ml in the 7th day and 7.8 micrograms/ml in the 30th day. No significant differences in the number of cardiac beats, or P-Q and Q-T intervals were found; there was no depression of sinus node function nor delay of AV conduction. In the basal state, ectopic supraventricular beats (105 +/- 20/24 hours) were observed in 7 patients and repetitive in five of them. In the first Holter ECG recording during CBZ treatment, a strong reduction of ectopic supraventricular beats (6 +/- 3/24 hours) and disappearance of the bursts was observed. In the second control, when the CBZ concentration was lower, the number of ectopic supraventricular beats were moderately increased (30 +/- 8/24 hours) and in one patient supraventricular tachycardia reappeared.CONCLUSIONSIn young epileptic subjects without signs of heart disease, CBZ seems to have no significant effect on conduction, yet has a possible antiarrhythmic effect.

The authors have studied the behaviour of ubidecorenone (Co Q10) in the acute phase of myocardial infarction in 24 patients, 19 male and 5 female, mean age 56.8 +/- 3.3. Ubidecorenone level was determined on admittance, after 48 hours and on the 7th and 30th days. A significant decrease was observed from the first to the 3rd day (mean values 0.90 +/- 0.18 microgram/ml vs 0.72 +/- 0.22, p less than 0.01). Thereafter a progressive rise was observed, but at the 30th day mean values were still below the basal ones. No significant differences were observed between patients treated with fibrinolytic agents and those not so treated, nor between those in whom reperfusion was obtained and the others. Nor was there a proven correlation with changes in creatinkinase. The behaviour of ubidecorenone may be associated with increased consumption for metabolic needs and increased destruction in scavenger action, and also to a lesser extent to decreased production due to lower food intake.

Annals of NeurologyVolume 29, Issue 5 p. 575-576 Letter Carbamazepine and the heart Mario Puletti MD, Mario Puletti MD II Clinica Medica, Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorCesare Iani MD, Cesare Iani MD Dipartimento di Scienze Neurologiche V Clinica Neurologica Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorMario Curione MD, Mario Curione MD II Clinica Medica, Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorMassimo Trappolini MD, Massimo Trappolini MD II Clinica Medica, Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorMario Manfredi MD, Mario Manfredi MD Dipartimento di Scienze Neurologiche V Clinica Neurologica Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this author Mario Puletti MD, Mario Puletti MD II Clinica Medica, Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorCesare Iani MD, Cesare Iani MD Dipartimento di Scienze Neurologiche V Clinica Neurologica Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorMario Curione MD, Mario Curione MD II Clinica Medica, Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorMassimo Trappolini MD, Massimo Trappolini MD II Clinica Medica, Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this authorMario Manfredi MD, Mario Manfredi MD Dipartimento di Scienze Neurologiche V Clinica Neurologica Università di Roma “La Sapienza” Rome, ItalySearch for more papers by this author First published: May 1991 https://doi.org/10.1002/ana.410290526Citations: 7AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Gasparetti CM. Conduction abnormalities complicating carbamazepine therapy. Am J Med 1987; 82: 381 2 Benassi E, Bo GP, Cocito L, et al. Carbamazepine and cardiac conduction disturbances. Ann Neurol 1987; 22: 280–281 3 Curione M, Iani C, Manfredi M, et al. Sino-atrial block by carbamazepine. J Neurol Neurosurg Psychiatry 1987; 50: 650 4 Takayanagi K, Yamaguchi H, Hayashi T, et al. Carbamazepine induced bradycardia-tachycardia syndrome with pharmacological analysis and concurrent ECG monitoring. J Electrocard 1990; 23: 85–88 5 Steinert C, Wit AL, Weiss MB, et al. The antiarrhythmic action of carbamazepine (Tegretol). J Pharmacol Exp Ther 1970; 173: 323–325 Citing Literature Volume29, Issue5May 1991Pages 575-576 ReferencesRelatedInformation

Nonrespiratory QRS amplitude variations related to PR interval length were observed in a case of complete atrioventricular (AV) block with narrow QRS complexes. This electrocardiographic pattern was studied, taking into consideration the greater deflection of the ventricular complexes (R- or S-wave) on each standard lead and by analyzing three groups of QRS (A,B,C) divided in relation to the different timing of the atrial systole. A significant variation appears in the entity of the mitral flow, as assessed by Doppler echocardiography evaluation, related to PR interval length, and a significant inverse correlation was found between QRS variability and ventricular diastolic filling.

In order to evaluate the incidence and prognostic significance of anterior precordial ST segment depression (decreases ST) in acute inferior myocardial infarction (MI), 158 patients with inferior MI were selected. In 90 patients (56.9%) an anterior decreases ST was associated with inferior lesion wave (group A), and in 68 patients (43.1%) only an ecg pattern of inferior myocardial infarction (group B) was present. No significant statistical differences were observed in mortality (group A 10% vs group B 10.2%), in compliances (group A 54.4% vs group B 47.0%) and in higher peak serum ck-levels (group A 83.3% vs group B 69.1%) in two groups during hospitalization period. In conclusion the anterior decreases ST during inferior MI should not be considered a negative prognostic sign. These favourable results are probably related to stringent criteria for ecg diagnosis of inferior myocardial infarction used and to exclusion of all patients with non contemporary evolution of anterior decreases ST and inferior lesion wave.

A study was carried out on 12 patients with wide QRS tachycardia, 8 of whom presented with atrioventricular (AV) dissociation (Group A) and 4 with 1:1 AV association (Group B). This investigation aimed at assessing whether significant variations occurred in the QRS amplitude between the two groups. Group A showed more marked variations in QRS amplitude (31.7 +/- 13%) compared to Group B patients (6.2 +/- 1.2%) (p less than 0.001). The amplitude changes observed in Group A patients are probably related to variations in telediastolic volume resulting from the occasional contribution of the atrial systole. The findings suggest that variability in QRS amplitude during wide QRS tachyarrhythmias is a reliable sign of the presence of an AV dissociation. The possibility of diagnosing an AV dissociation on a surface ECG without visible P waves is an important finding, which though not pathognomonic of ventricular tachycardia, is a valid ECG criterion for assessing the ventricular origin of arrhythmias. This ECG criterion can be usefully applied in clinical practice along with others already used for the differential diagnosis of wide QRS tachyarrhythmias.