Ventricular late potentials and ventricular arrhythmias in noncoronarogenic myocardial diseases

Hemodynamic parameters and survival were studied in 48 patients with noncoronarogenic myocardial diseases (NCMD). The examination included high-resolution electrocardiography and Holter monitoring of cardiac rhythm. Deterioration of pump capacity of the heart was associated with high-grade arrhythmias (4B and higher) while ventricular late potentials were more characteristic for patients with severe hemodynamic disorders and, in particular, with dilated cardiomyopathy. The prognosis in NCMD is based on clinical evidence on functional class of the heart failure, parameters of central and intrapulmonary hemodynamics.     

Ventricular arrhythmias in the elderly

Sudden cardiac death is one of the leading causes of death and a major public health problem that particularly affects the elderly. Sudden cardiac death may be a terminal event after a prolonged debilitating and painful illness, or it may occur following many years of symptoms related to a cardiac disorder; however, in many elderly persons, the cardiac arrest may be the first manifestation of cardiac disease in a supposedly healthy and physically active person. Whether cardiopulmonary resuscitation should be performed in elderly patients who sustain cardiac arrest is a significant issue confronting the medical profession and the general public. Several questions must be answered when evaluating the decision of whether or not to perform cardiopulmonary resuscitation on an elderly patient.     

Ventricular arrhythmias and sudden cardiac death in acute myocardial infarct in the era of thrombolytics

Sudden cardiac death (SCD) in the setting of acute myocardial infarction (AMI) remains an actual problem. There is a very close relationship between ventricular arrhythmias and SCD in AMI. Malignant ventricular arrhythmias, such as ventricular fibrillation and ventricular tachycardia are the major causes of SCD in coincidence with AMI. Frequent and complex ventricular arrhythmias are also important predictors of the risk of SCD in coincidence with and after AMI. In this article the authors emphasize the importance of the complexity of pathophysiological mechanisms responsible for the genesis of ventricular arrhythmias in coincidence with AMI. The necessity of taking into account the current knowledge about pathophysiology in prevention and therapy of separate forms of ventricular arrhythmias is also emphasized. The incidence and time course of ventricular arrhythmias and SCD in coincidence with AIM in prethrombolytic and thrombolytic periods is described. The importance of separate forms of ventricular arrhythmias in coincidence with AMI with regard to short and long-term prognoses is described. There are discussed also the possible mechanisms of thrombolytic and adjuvant therapies that affect the incidence and frequency of ventricular arrhythmias. The authors recommend the optimal therapy for each form of ventricular arrhythmia and the following management of patients with AMI. In the prevention and therapy of ventricular arrhythmias in the setting of AMI the authors emphasize the importance of early recanalization and prevention of re-occlusion of the infarction-related coronary artery. Great importance is attributed also to other adjuvant measures directed to the restriction of the size of infarction, myocardium protection, prevention and attenuation of remodelling of the left ventricle and thereby to the prevention of heart failure and attenuation of adverse effects of the sympathetic nervous system. An early administration of beta-blockers which favourable effect in and after AMI was documented with conclusive evidence is considered as one of the most important measures in prevention and therapy of malignant ventricular arrhythmias and SCD. The occurrence of malignant ventricular arrhythmias in the setting of heart failure and/or 24-48 hours after AMI should be an indication for aggressive management directed to arrhythmia (programmed ventricular stimulation, electrophysiologically guided pharmacologic or nonpharmacologic therapy) as well as to underlying coronary heart disease (coronary angiography and revascularization).     

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)     

Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias

Cultivated sugarcane clones (Saccharum spp., 2n=100 to 130) are derived from complex interspecific hybridizations between the species S. officinarum and S. spontaneum. Using comparative genomic DNA in situ hybridization, we demonstrated that it is possible to distinguish the chromosomes contributed by these two species in an interspecific F1 hybrid and a cultivated clone, R570. In the interspecific F1 studied, we observed n + n transmission of the parental chromosomes instead of the peculiar 2n + n transmission usually described in such crosses. Among the chromosomes of cultivar R570 (2n = 107-115) about 10% were identified as originating from S. spontaneum and about 10% were identified as recombinant chromosomes between the two species S. officinarum and S. spontaneum. This demonstrated for the first time the occurrence of recombination between the chromosomes of these two species. The rDNA sites were located by in situ hybridization in these two species and the cultivar R570. This supported different basic chromosome numbers and chromosome structural differences between the two species and provided a first bridge between physical and genetical mapping in sugarcane.     

Insulin induces medial hypertrophy of myocardial arterioles in rats

To investigate the effect of hyperinsulinemia on arteriolar hypertrophy, myocardial hypertrophy, and blood pressure, we administered insulin intraperitoneally to SHR and WKY rats for 3 consecutive weeks. To prevent hypoglycemia, the drinking water contained 10% sugar, and to accentuate the blood pressure, their chow contained 8% table salt. Blood pressure was measured by the tail-cuff method. Heart weights were factored with body weights. Arterioles of approximately 100 microns in diameter were examined at the end of the experiment and the vascular wall thickness was factored with the lumen diameter. At the end of 3 weeks, blood pressure rose in the SHR but not in the WKY rats. The heart weights in the WKY normotensive rats did not increase, whereas in the SHR they did. Furthermore, there was a significant rise in vessel wall thickness in the rats that received insulin, whether there was a rise in blood pressure or not and whether they had an increase in heart weight or not. There was a similar rise in blood glucose in all the groups, with slightly more accentuated rise in the SHR that received insulin. Nevertheless the increase in vascular wall thickness occurred only in the groups which received insulin. This seems to preclude the importance of hyperglycemia per se as the causative agent for the increase in vascular wall thickness in this study. The increase was in the form of medial hypertrophy without any sign of atherosclerosis. It seems, therefore, that hyperinsulinemia is associated with hypertrophy of the media of arterioles regardless of the increase in heart weight or the rise in blood pressure.     

Increased prevalence of cardiac arrhythmias and transient episodes of myocardial ischemia in hypertensives with left ventricular hypertrophy but without clinical history of coronary heart disease

To evaluate the behavior of cardiac arrhythmias (CA) and transient episodes of myocardial ischemia (TEMI), in relation to the circadian pattern of blood pressure in patients suffering from arterial hypertension, with or without echocardiographically ascertained left ventricular hypertrophy (LVH), we studied 128 patients, 87 men (M) and 41 women (F), aging from 21 to 76 years, subdivided into two groups: Group I, including 66 patients with LVH (45 M and 21 F; mean age of 53.7 +/- 9.1 years; Group II, including 62 patients without LVH (42 M and 20 F; mean age of 49.7 +/- 9.5 years). Office blood pressure (OBP) as well as nighttime ambulatory blood pressure (ABP) were higher in patients with LVH (P < .05 and P < .01). CA were present in a higher number of patients of Group I (P < .001): premature supraventricular beats (PSVB) 22.7 v 4.8%, supraventricular couplets (SVC) 36.4 v 16.1%, supraventricular tachycardia runs (SVT runs) 27.3 v 12.9%, ventricular ectopic beats (VEB) 25.6 v 8.0%, ventricular couplets (VC) 30.3 v 12.9%, ventricular tachycardia runs (VT runs) 12.1 v 3.2%. The absolute number of ectopic beats was also significantly higher in patients of Group I. Ventricular arrhythmias were significantly related to ASBP (r = 0.83, P < .01), to ADBP (r = 0.74, P < .01) and to heart rate (r = 0.87, P < .01) in patients of Group I. TEMI were more frequent in patients of Group I (73 v 41 episodes, 39.39% v 25.8% of patients, P < .01) and were related to ABP peaks. In fact, in both groups of patients all TEMI without heart rate increase and most TEMI with heart rate increase were registered between 6:00 and midnight, hours in which ABP values were higher. We conclude that hypertensives with LVH, but without clinical history of coronary heart disease, have a higher prevalence of ventricular arrhythmias and of transient episodes of myocardial ischemia in relation to the circadian pattern of ABP.     

Silent myocardial ischaemia and left ventricle hypertrophy in diabetic patients

The purpose of this study was to evaluate the ability of three noninvasive techniques to detect silent myocardial ischaemia and analyse the factors associated with this condition, particularly left ventricular hypertrophy, in diabetic patients. An ECG stress test, a thallium-201 myocardial scintigraphy with dipyridamole intravenous infusion, ambulatory 48 h ECG monitoring and an echocardiographic study were performed in 92 diabetic patients without cardiac symptoms but with > or = 2 additional cardiovascular risk factors. At least one of these tests was positive in 28 patients (30.4%), suggesting silent myocardial ischaemia. Twenty-four of these patients had a coronary angiography which showed significant coronary stenosis in only 9 cases. An accurate echocardiographic tracing was obtained in 79 patients, particularly in 7 of the 9 with coronary stenosis. Left ventricular hypertrophy was detected in 34 patients, 6 of whom had coronary stenosis. In patients with left ventricular hypertrophy, the positive predictive values of myocardial scintigraphy and the ECG stress test were respectively 50% and 100%, as compared to only 33% and 11% in those without hypertrophy. In summary, coronary stenoses were found in < 10% of asymptomatic diabetic patients with > or = 2 cardiovascular risk factors, but more frequently in individuals with left ventricular hypertrophy. Thus, silent myocardial ischaemia should be searched for first in diabetic patients with hypertrophy, for which the stress test was the most accurate detection method in this study.     

Role of cardiac renin-angiotensin system in swimming induced physiological myocardial hypertrophy

To determine the contribution of cardiac renin-angiotensin system (RAS) to the physiological myocardial hypertrophy induced by swimming training and the relationship between locally produced and circulating RAS, both ventricular and plasma angiotensin (Ang) I and II contents, ventricular angiotensin converting enzyme (ACE) and plasma renin activity (PRA) were detected by means of radioimmunoassay and biochemical method. It was shown that after 5 weeks of swimming, the ventricular wet weight to body weight ratio (V/Bwt) and Ang II in both left and right ventricles and ACE activity increased markedly as compared with the controls (P < 0.05). Furthermore, significantly positive correlation was found between the ventricular Ang II and V/Bwt (r = 0.7721, P < 0.001), while the plasma Ang I and II and PRA remained at the control level. No correlation was found between plasma Ang II and V/Bwt. These above findings suggest that cardiac RAS may play an important role in physiological myocardial hypertrophy and to a large extent is in dependent on circulating RAS.     

Postoperative arrhythmias and myocardial electrolytes in patients undergoing coronary artery bypass grafting

Electrolyte changes in right atrial and skeletal muscle pre- intra- and postoperatively, and their relationship to the development of postoperative atrial fibrillation or flutter were evaluated in 31 patients with coronary artery bypass grafting (CABG). Such postoperative arrhythmias occurred in 14 patients (45%). Before CABG the skeletal muscle potassium concentration was lower in these patients than in the others: median 261.4 (range 148.2-329.5) vs 298.6 (167.1-416.4) mumol/g dry weight, p = 0.017. The right atrial potassium concentration was normal, but sodium levels were higher in the patients with, than in those without postoperative arrhythmias: median 340.3 (263.7-454.9) vs 296.3 (203.9-355.0) mumol/g dry weight, p = 0.008, indicating disturbed transmembrane electrolyte transfer. During CABG the potassium levels fell and sodium increased in both right atrium and skeletal muscle, and on postoperative day 2 the potassium content in skeletal muscle was not yet restored. Magnesium levels showed no changes in right atrium or skeletal muscle, but serum magnesium declined postoperatively. As the observed electrolyte derangements may be important in the development of postoperative arrhythmias, concomitant potassium and magnesium supplement postoperatively may be beneficial in restoring cellular potassium concentration.     

Cardiac hypertrophy alters myocardial response to ischaemia and reperfusion in vivo

The impact of cardiac hypertrophy on myocardial biochemical and physiological responses to ischaemia-reperfusion (I-R) was investigated in vivo. Hypertrophy was produced by aortic constriction (PH) or swimming training (TH). Open-chest rat hearts in PH, TH and a sedentary control group (SC) were subjected: (1) to ischaemia, by surgical occlusion of the main descending branch of the left coronary artery for 30 min; (2) to I-R, by releasing the occluded blood vessel for 15 min; or (3) to a sham operation. Ischaemia per se had little effect on heart oxidative and antioxidant status, or lipid peroxidation. However, I-R significantly decreased glutathione (GSH) content, increased glutathione disulfide (GSSG) content, and reduced GSH/GSSG ratio in the SC hearts. These alterations were associated with decreased activities of GSH peroxidase and GSSG reductase, and an increase in lipid peroxidation. Myocardial ATP, total adenine nucleotide content and energy charge in SC were significantly decreased after ischaemia, whereas levels of purine nucleotide derivatives, particularly adenosine, were elevated. No significant alteration of GSH status of adenine nucleotide metabolism occurred after ischaemia or I-R in hypertrophied hearts. In both PH and TH, glutathione content was significantly higher than in SC, whereas activities of GSH peroxidase and GSSG reductases were lower. TH rats maintained a higher heart rate (HR), peak systolic pressure, and energy charge during I-R. These data indicate that hypertrophied but well-functioned hearts may be more resistant to I-R induced disturbances of myocardial oxidative and antioxidant functions.     

Ventricular arrhythmias in syndrome of balloon deformity of mitral valve. Definition of possible high risk group

Twenty patients clinically identified as having balloon deformity of the mitral valve were studied to assess the incidence of ventricular arrhythmias. Echocardiography and phonocardiography were used to confirm the nature of the mitral valve lesion. Continuous 24-hour electrocardiograms were obtained from all patients and analysed by a computer and 2 observers. One patient has ventricular fibrillation and 3 patients had ventricular tachycardia. There was a high incidence of other less severe forms of ventricular arrhythmias. Eight patients had inferolateral ST and T wave abnormality on the resting electrocardiogram, and were described as having the ausculatatory-electrocardiographic variant of the balloon mitral valve syndrome. The occurrence of serious ventricular arrhythmias (ventricular fibrillation and tachycardia) was significantly more frequent in this group. This raises the possibility that the resting electrocardiogram may identify those patients with balloon deformity of the mitral valve who are at risk from sudden death.     

Regression of left ventricular hypertrophy prevents ischemia-induced lethal arrhythmias. Beneficial effect of angiotensin II blockade

To evaluate the preventive effect of regression of left ventricular hypertrophy (LVH) on sudden cardiac death (SCD), the incidence of ventricular tachycardia or ventricular fibrillation (VT/Vf) after left coronary artery occlusion in Langendorff preparations was studied in the following five groups: (1) spontaneously hypertensive rats (SHR) without treatment (SHR-N), (2) SHR treated with captopril (SHR-C), (3) SHR treated with the angiotensin II receptor antagonist TCV-116 (SHR-A), (4) SHR treated with hydralazine (SHR-H), and (5) Wistar-Kyoto (WKY) rats. Although blood pressure was equally lowered in all treated groups, SHR-C and SHR-A but not SHR-H showed regression of LVH. The incidence of VT/Vf was 5% in WKY rats, 63% in SHR-N (P < .005 versus WKY rats), 0% in SHR-C, 10% in SHR-A, and 45% in SHR-H (P < .05 versus WKY rats). Further evaluation of the effect of TCV-116 revealed that SHR treated with a low dose of TCV-116 (1 mg/kg per day) showed a decrease in left ventricular mass with only a little decrease in blood pressure and that the incidence of VT/Vf was reduced in association with the degree of regression of LVH. Electrophysiological study using microelectrode techniques revealed that in the LVH groups (SHR-N and SHR-H), the action potential duration (APD) of the left ventricular papillary muscle was more prolonged than in WKY rats, whereas APD shortened to a greater extent during superfusion with a hypoxia/no-glucose solution. APD showed no difference in the regression groups (SHR-C and SHR-A) compared with the WKY group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Conduction system in fatal myocardial sarcoidosis with variegated arrhythmias (author''s transl)

We present four cases of non-instrumental traumatic ruptures of the hypopharynx and the esophagus. Three are ruptures with closed neck and one with a rupture associated with a cervical wound. A conjoined lesion of the airway is usual, except in one of our observation. All people injured come from car, sport, or work accidents. The esophageal wound, contaminating the mediastinum, is life-threatening and requires a rapid therapeutic solution: wide drainage tube and antibiotics. The diagnosis, often difficult due to poor symptomatology, must be thought of when there is any severe trauma of the cervical region.     

Effects of guan-fu base a on experimental cardiac arrhythmias and myocardial contractility

Guan-fu base A (GFA) is a terpenoid alkaloid isolated from the tuber of Aconitum coreanum in our institute. GFA (20-30 mg.L-1) reduced the ventricular tachycardia (VT) and ventricular fibrillation (VF) rate induced by K(+)-free and high Ca2+ solution in Langendorf heart of rats. Pretreatment of conscious rats with GFA 2.5-10 mg.kg-1 iv, increased the amount of beiwutine necessary to produce arrhythmias. Ouabain-induced VT in conscious dogs was reverted to sinus rhythm in 1-2 min by iv GFA 9-10 mg.kg-1. GFA 10-20 mg.kg-1 iv was also found to be effective in protecting anesthetized dogs from atrial fibrillation induced by topical application of ACh. GFA 10 mg.kg-1 iv obviously decreased heart rate and prolonged the P-R interval, but slightly affected the myocardial contractility in anesthetized dogs. GFA showed no obvious effect on stroke volume and cardiac output in conscious dogs. In conclusion, GFA showed therapeutic and prophylactic effect on different models of experimental arrhythmias without causing marked effect on myocardial contractility.     

Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy

Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide-binding (G) protein. For example, several receptors that couple to Gq class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of Gq-mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carboxyl-terminal peptide of the alpha subunit Galphaq. When pressure overload was surgically induced, the transgenic mice developed significantly less ventricular hypertrophy than control animals. The data demonstrate the role of myocardial Gq in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to Gq.