Intra-atrial Conduction Disturbances Research Articles

Characterization of mid-term atrial geometrical and electrical remodeling following device closure of atrial septal defects in adults

PurposeLate-onset atrial arrhythmia after successful closure of atrial septal defect (ASD) is not uncommon. Right atrial (RA) enlargement and increased electrocardiographic P-wave dispersion (Pd) independently predict the development of atrial arrhythmia. Data on the degree of right atrial (RA) geometrical and electrical remodeling following device closure of ASD are limited. MethodsEchocardiography and electrocardiography (ECG) were performed in 58 consecutive patients (47±17years) before and at 3months after ASD closure. Persistent RA enlargement was defined as RA volume index (RAVI) ≥21ml/m2 at 3months. Pd was calculated as the difference between maximal and minimal P-wave durations in 12-lead ECG. ResultsRA size reduced (RAVI: 50±28 vs. 26±16ml/m2, p<0.001) and Pd on ECG decreased (53±17 vs. 49±20ms, p<0.05) significantly at 3months when compared to baseline. However, persistent RA enlargement remained evident in 31 patients (53%). As a group, they were older with higher pulmonary arterial systolic pressure, larger Qp/Qs, longer maximal P-wave duration and Pd than those with normalized RA. Pd reduction only occurred in patients with normalized RA size. The 3-month Pd (hazard ratio: 1.033, p<0.001) predicted the presence of incomplete RA geometrical remodeling. ROC curve revealed that Pd ≥45ms at 3months was 77% sensitive and 86% specific in revealing residual RA enlargement. ConclusionBoth atrial geometrical and electrical reverse remodeling were evident at 3months following ASD closure. However, only half of the included patients had normalization of RA size which could be revealed by a simple ECG surrogate of intra-atrial conduction disturbance.

Atrium-Atrioventricular Node Conduction Block during Catheter Ablation of Persistent Atrial Fibrillation.

Previous studies have suggested that fibrillatory substrates are widely distributed in both atria in patients with persistent atrial fibrillation. Extensive bi-atrial ablation has been increasingly performed to improve the clinical outcomes; however, this may adversely affect the intra-atrial conduction during sinus rhythm. The worst con- sequence of an intra-atrial conduction disturbance is conduction block between the atrium and atrioventricular node. There have been a few case reports on this complication, which suggest that the conduction block may occur more. This review aimed to describe the risk factors and method of prevention of atrium-atrioventric-ular node conduction block.

Caso 3/2008: dispnéia intensa rapidamente progressiva em mulher portadora de prótese mecânica em posição mitral

The patient was discharged with warfarin and was sent for clinical follow-up in the city where she had been referred from. She had recurrent dyspnea on heavy exertion eight years after A 58-year-old woman sought hospital care for dyspnea on minimum exertion felt for three days. At 34 years of age, two months after an episode of arthritis of her right ankle, which was treated with prednisone, the patient developed tiredness on heavy exertion such as climbing up a slope or carrying weight. Then she developed palpitations. On physical examination, at that time, her weight was 69.2 kg, her height was 1.63m, body mass index of 26 kg/m2, regular pulse of 78 beats per minute, and blood pressure of 120/70 mmHg. Lung examination was normal. Heart examination was significant for apical impulse in the fifth left intercostal space at the midclavicular line. Intensity of S1 was diminished in the mitral area, intensity of S2 was normal in the pulmonic and aortic areas. A grade 1 systolic murmur and grade 1 late diastolic murmur in the mitral area were observed. Abdominal examination was normal. The electrocardiogram (3/25/1981) showed normal sinus rhythm, ventricular extrasystoles, P wave duration of 80 ms, PR-interval duration of 160 ms, QRS duration of 80 ms, SÂP – 60o and SÂQRS 60o. P wave morphology denoted intra-atrial conduction disturbance (Figure 1). Echocardiogram (04/01/1981) showed enlarged left atrium as well as mitral valve commissural fusion and thickening (Table 1). The patient was diagnosed with rheumatic mitral stenosis. She was started on daily doses of amiodarone 200 mg and chlorthalidone 50 mg (which she did not tolerate). She had follow-up visits in 05/05/1982, 09/06/1982, 03/07/1983 in which she was clinically stable. During the follow-up her electrocardiogram (09/08/1982) showed atrial fibrillation and an inactive interventricular septal Figure 1 ECG. Signs of Probable left atrial overload.

AGEs‐RAGE System Mediates Atrial Structural Remodeling in the Diabetic Rat

Diabetes mellitus (DM) is one of the independent risk factors for atrial fibrillation (AF). Our previous study has indicated that DM causes atrial structural remodeling with intraatrial conduction disturbances. We tested the hypothesis that the advanced glycation end products (AGEs) and the receptor for AGE (RAGE), which have been implicated in diabetic complications, are responsible for the atrial structural remodeling. Diabetes was induced by streptozotocin (65 mg/kg i.p.) in 8-week-old female Sprague-Dawley rats. When 24 weeks old, their atria were subjected to histology, Western blotting, and immunohistochemistry. The HbA(1c) value of induced-DM rats was significantly higher than that of control rats. Histological and immunohistochemical examinations revealed that the atria of diabetic rats showed remarkable structural changes characterized by diffuse interstitial fibrosis with abundant expressions of RAGE and connective tissue growth factor (CTGF), which findings were also confirmed by Western blotting analysis. This diabetes-induced atrial fibrosis was remarkably prevented by administration of an inhibitor of AGEs formation, OPB-9195, along with reduction of CTGF expression. DM promoted atrial structural remodeling via the activation of the AGEs-RAGE system with upregulating CTGF. The inhibition of AGEs formation could be a novel upstream therapeutic approach for diabetes-related atrial fibrosis.

Posttraumatic Period in Cardiac Contusion (Experimental Study)

Objective: to study the efficiency of pre-administration of hypoxen in experimental cardiac contusion in order to lower the degree of posttraumatic myocardial dysfunction. Materials and methods: experiments were carried out on non-inbred albino male rats anesthetized with sodium thiopental. Cardiac contusion was reproduced by an original device that imitated a blow of the steering wheel to the anterior chest, as that observed when a moving car clashes against an obstacle. Some animals were traumatized after pre-administration of hypoxen. An electrocardiogram, left carotid blood pressure (BP), an integral rheogram, and the first derivative of a differential rheogram were recorded prior to cardiac contusion simulation and in different posttraumatic periods. Stroke volume (SV), cardiac output (CO), and total peripheral vascular resistance were calculated. Results. Preinjection of hypoxen completely prevented the development of sinus arrhythmia, paroxysmal ventricular tachycardia, and intraatrial and intraventricular conduction disturbances, irrespective of the baseline BP. In a subgroup of animals with a baseline low BP, the agent reduced the incidence of bradycardia by 1.5 times, heterotopic rhythms by 5.3 times, ventricular premature contractions by 6 times, atrioventricular (AV) block by 5.3 times and diminished the changes in the terminal of a ventricular complex by 6.3 times. In a subgroup of animals with baseline normal BP, bradycardia and heterotopic rhythms were recorded 2 and 7 times more infrequently recorded; ventricular premature beats, AV block, and ST-segment displacement were present in none case. Preinjection of hypoxen improved myocardial contractility, as evidenced by 17—25% SV increases within an hour posttraumatically. However, significant arterial hypotension and lowered CO due to bradycardia in most experimental animals during the preinjection of hypoxen before injury and throughout the posttraumatic period caused a ten-fold increase in mortality rates as compared with the non-hypoxen group. Conclusion. The hemodynamic effects of hypoxen can substantially limit the possibility of using the agent to diminish the degree of posttraumatic cardiac dysfunction. Key words: experimental cardiac contusion, central hemodynamics, hypoxen.

P wave dispersion is prolonged in patients with Wilson’s disease

To investigate the P wave dispersion as a non-invasive marker of intra-atrial conduction disturbances in patients with Wilson's disease. We compared Wilsonos disease patients (n = 18) with age matched healthy subjects (n = 15) as controls. The diagnosis was based on clinical symptoms, laboratory tests (ceruloplasmin, urinary and hepatic copper concentrations). P wave dispersion, a measurement of the heterogeneity of atrial depolarization, was measured as the difference between the duration of the longest and the shortest P-waves in 12 lead electrocardiography. All the patients were asymptomatic on cardiological examination and have sinusal rhythm in electrocardiography. Left ventricular and left atrial diameters, left ventricular ejection fraction and left ventricular mass index were similar in both groups. The Wilson's disease patients had a significantly higher P wave dispersion compared with the controls (44.7 +/- 5.8 vs 25.7 +/- 2.5, P < 0.01). There was an increase in P wave dispersion in cardiologically asymptomatic Wilson's disease patients which probably represents an early stage of cardiac involvement.

The Intra-atrial Conduction Disturbance in Brugada Syndrome Patients with Atrial Fibrination

The Intra-atrial Conduction Disturbance in Brugada Syndrome Patients with Atrial Fibrination

What are Arrhythmogenic Substrates in Diabetic Rat Atria?

Diabetes mellitus is one of the significant independent risk factors for the development of atrial fibrillation (AF). However, the pathophysiological mechanisms of the relationship have not been fully elucidated. The genetic type II diabetes (GK) rats and their original (Wistar) ones were subjected to electrophysiological (n = 8 per group) and histological (n = 7 per group) studies. At 40 weeks old, when GK rats had significantly (P < 0.01) more increased plasma glucose and HbA(1c) values than Wistar rats, atrial electrical stimuli in the isolated-perfused hearts induced significantly greater number of repetitive atrial responses in GK rats than in Wistar rats (47.9 +/- 17.5 vs 3.1 +/- 1.3 beats, respectively, P < 0.01). GK rats showed significantly longer intra-atrial activation time than Wistar rats (18.3 +/- 0.4 ms vs 15.9 +/- 0.5 ms, P < 0.01) without any significant difference in the atrial refractoriness. The histological examination revealed significantly increased diffuse fibrotic deposition in GK rats atria compared with Wistar ones (P < 0.01). The present diabetic GK rat showed increased atrial arrhythmogenicity with intra-atrial conduction disturbance, and thus indicated that the structural remodeling of atrium characterized by diffuse interstitial fibrosis would be a major substrate for diabetes-related AF.

Electrical, contractile and structural remodeling during atrial fibrillation.

The natural history of atrial fibrillation (AF) is characterized by a gradual worsening with time. The recent finding that AF itself produces changes in atrial function and structure has provided a possible explanation for the progressive nature of this arrhythmia. Electrical remodeling (shortening of atrial refractoriness) develops within the first days of AF and contributes to an increase in stability of AF. However, 'domestication of AF' must also depend on a 'second factor' since the persistence of AF continues to increase after electrical remodeling has been completed. Atrial contractile remodeling (loss of contractility) leads to a reduced atrial transport function after cardioversion of AF. An important clinical consequence is that during several days after restoration of sinus rhythm, the risk of atrial thrombus formation is still high. In addition, the reduction of atrial contractility during AF may enhance atrial dilatation which may add to the persistence of AF. Tachycardia-induced structural remodeling takes place in a different time domain (weeks to months). Myolysis probably contributes to the loss of atrial contractile force. Although it might explain the loss of efficacy of pharmacological cardioversion and the development of permanent AF, the role of structural remodeling in the progression of AF is still unclear. Atrial structural remodeling also occurs as a result of heart failure and other underlying cardiovascular diseases. The associated atrial fibrosis might explain intra-atrial conduction disturbances and the susceptibility for AF. Thus, both AF itself and the underlying heart disease are responsible for the development of the arrhythmogenic substrate. New strategies for prevention and termination of AF should be build on our knowledge of the mechanisms and time course of AF-induced atrial remodeling.

Atrial activation during sinus rhythm in patients with rheumatic and non-rheumatic paroxysmal atrial fibrillation. Frequency-domain analysis using signal-averaged electrocardiography.

Using P-wave signal-averaged electrocardiography, we assessed the patterns of atrial electrical activation in patients with idiopathic atrial fibrillation as compared with patterns in patients with atrial fibrillation associated with structural heart disease. Eighty patients with recurrent paroxysmal atrial fibrillation were divided into 3 groups as follows: group I - 40 patients with atrial fibrillation associated with non-rheumatic heart disease; group II - 25 patients with rheumatic atrial fibrillation; and group III - 15 patients with idiopathic atrial fibrillation. All patients underwent P-wave signal-averaged electrocardiography for frequency-domain analysis using spectrotemporal mapping and statistical techniques for detecting and quantifying intraatrial conduction disturbances. We observed an important fragmentation in atrial electrical conduction in 27% of the patients in group I, 64% of the patients in group II, and 67% of the patients in group III (p=0.003). Idiopathic atrial fibrillation has important intraatrial conduction disturbances. These alterations are similar to those observed in individuals with rheumatic atrial fibrillation, suggesting the existence of some degree of structural involvement of the atrial myocardium that cannot be detected with conventional electrocardiography and echocardiography.

Pace prevention of atrial fibrillation: what can we expect from new algorithms?

Since the observation that antibradycardia pacing may prevent vagal-mediated parosysmal atrial fibrillation, several approaches have been undertaken to establish pace-prevention of atrial fibrillation as a therapeutic option in such patients. Multisite pacing strategies like biatrial, bifocal right atrial or septal pacing are in first line so-called substrate-modulators of atrial fibrillation that try to compensate for inter- and intraatrial conduction disturbances. Preventive pacing algorithms, which can be used with a conventional atrial lead position, are designed to suppress premature atrial contractions and salvos as a known trigger of atrial fibrillation. Pace conditioning: This algorithm adjusts the rate just above the intrinsic sinus rate with the aim to overdrive and pace the atrium for at least 95% of the time. Premature atrial contraction suppression: When a spontaneous atrial event is classified as a premature atrial contraction, the pacing rate is increased to 15 min-1 above the physiological rate and kept stable for a certain period. Post-premature atrial contraction response: This algorithm is designed to prevent arrhythmogenic pauses after premature atrial contractions by controlling the atrial rate only in the two beats after each premature atrial contraction. Post-exercise response: The post-exercise pacing rate is adjusted to both the level and the duration of exercise in order to prevent too step of a rate drop at the onset of the recovery phase. These four preventive pacing algorithms are currently investigated in the AFtherapy study. The results of this and other prospective pacing studies will not only clarify the relevance and effectiveness of pacing for prevention of atrial fibrillation but will also enlarge our knowledge about the induction mechanisms of atrial fibrillation in patients.

Conduction disturbances and increased atrial vulnerability in Connexin40-deficient mice analyzed by transesophageal stimulation.

Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. Fifty-two mice (18 Cx40(+/+), 15 Cx40(+/-), and 19 Cx40(-/-) mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40(-/-) mice compared with Cx40(+/-) and Cx40(+/+) mice (287.8+/-109.0 vs 211.1+/-61.8 vs 204.4+/-60.9 ms; P<0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40(-/-) mice than in Cx40(+/-) or Cx40(+/+) mice (93. 3+/-11.8 vs 83.9+/-9.7 vs 82.8+/-8.0 ms, P<0.05). Analysis of 27 Cx40(-/-) mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40(+/-) and 31 wild-type (Cx40(+/+)) mice. Furthermore, in Cx40(-/-) mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis.

Cardiac arrhythmias in Chagas' heart disease.

Chagas' disease is a chronic parasitosis affecting most Latin American countries. Its most important clinical manifestation is a late developing chronic myocarditis and, much less frequently, an early acute myocarditis. Chagasic myocardial damage is microfocal and disseminated throughout the heart. In most cases, the coexistence of areas of myocytic degeneration, inflammatory infiltration, and fibrosis suggests a permanent evolving process. Commonly, chronic chagasic myocarditis resembles a dilated cardiomyopathy, with characteristic ECG abnormalities (atrial and ventricular extrasystoles, intraventricular and/or AV conduction disturbances, and primary ST-T wave changes). Since myocardial damage is scattered throughout the heart, the ECG abnormalities (arrhythmias, conduction disturbances, and repolarization changes) are also representative of the widespread cardiac involvement. Thus, sick sinus syndrome, atrial extrasystoles, intraatrial conduction disturbances, and atrial fibrillation or flutter are common findings in different stages of the disease. At the ventricular level, both conduction disturbances and arrhythmias are conspicuous expressions of the myocardial damage. Right bundle branch block alone or in combination with left anterior hemiblock are the most common conduction defects. Further compromise of the conduction system can lead to different degrees of AV block. Chagas' disease is the main cause of bundle branch block and AV block in endemic areas. In advanced cases of Chagas' heart disease, ventricular premature contractions are extremely frequent, multiform, and repetitive (couplets and runs of ventricular tachycardia), and show R on T phenomenon. These arrhythmias are usually aggravated by increased sympathetic tone, implying an enhanced risk of cardiac sudden death among chagasic patients, which is sometimes the first manifestation of the illness. Chronic chagasic myocarditis is the leading cause of cardiovascular death, mostly as a consequence of heart failure and sudden death, in areas where the disease is endemic.

Simulated myocardial infarction and slow atrial flutter due to cerebral embolism from a free left atrial thrombus.

The case of a 38-year-old female who suffered a cerebral embolism from a free left atrial thrombus is reported. The clinical picture, including serum enzyme elevations, was consistent with a nontransmural myocardial infarction. Atrial flutter exhibiting very slow (162/min) and tall waves was transiently recorded indicating development of an intra-atrial conduction disturbance.

Transient Complete AV Block in Lyme Disease: Electrophysiologic Observations

The findings in a patient with complete AV block and intra-atrial conduction disturbances due to Lyme disease are presented. The electrocardiographic follow-up and serial EP findings suggest that complete AV block in Lyme disease may signify a more extensive affection of the AV conduction system (with eventually attendant intra-atrial conduction disturbances) than described in earlier reports. An almost complete resolution of the considerable damage to the conduction system occurred within two weeks.

Criteria for intraventricular conduction disturbances and pre-excitation

In an effort to standardize terminology and criteria for clinical electrocardiography, and as a follow-up of its work on definitions of terms related to cardiac rhythm, an Ad Hoc Working Group established by the World Health Organization and the International Society and Federation of Cardiology reviewed criteria for the diagnosis of conduction disturbances and pre-excitation. Recommendations resulting from these discussions are summarized for the diagnosis of complete and incomplete right and left bundle branch block, left anterior and left posterior fascicular block, nonspecific intraventricular block, Wolff-Parkinson-White syndrome and related pre-excitation patterns. Criteria for intraatrial conduction disturbances are also briefly reviewed. The criteria are described in clinical terms. A concise description of the criteria using formal Boolean logic is given in the Appendix. For the incorporation into computer electrocardiographic analysis programs, the limits of some interval measurements may need to be adjusted.

Effect of ouabain on electrical coupling of rabbit atrial muscle fibers.

The effects of ouabain on passive electrical properties of isolated rabbit atrial muscle fibers (crista-terminalis) were investigated. The space constant as well as the time constant of the crista-terminalis was determined using the partition method of Kamiyama and Matsuda based on the cable equation proposed by Hodgkin and Rushton. Ouabain treatment for 30 minutes at a lower concentration (2 X 10(-7) M), caused no significant change in the space constant and time constant of the crista-terminalis. After ouabain treatment for 30 minutes at a higher concentration (1 X 10(-6) M), the space constant of the crista-terminalis was reduced significantly, whereas the time constant was not affected. An apparent reduction in the resting membrane potential and the amplitude of action potential was also observed at the higher concentration of ouabain. These effects of ouabain on passive electrical properties of the crista-terminalis are most likely explained by the increase of its axial resistance (electrical uncoupling) due to intracellular calcium accumulation resulting from inhibition of the membrane sodium pump. This suggests that such an electrical uncoupling may play an important role in the intra-atrial conduction disturbance by cardiac glycosides.

Reversed Sequential Activation of the Atria: Vectorcardiographic and External Pulse Wave Features

Limitations of the electrocardiogram for the diagnosis of atrial enlargement and defects in atrial conduction are well recognized. High-magnification vectorcardiography has proven very useful for establishing the diagnosis of atrial enlargement 1 Benchimol A Desser KB Tio S et al. Vectorcardiographic diagnosis of atrial hypertrophy. in: Hoffman I Hamby RI Vectorcardiography 3. North-Holland Publishing Co, Amsterdam1976: 75-85 Google Scholar and in defining various types of disturbances in intra-atrial conduction, either associated with atrial hypertrophy or enlargement or as isolated findings. 2 Zoneraich O Zoneraich S The P-loop in intra-atrial conduction disturbances. in: Hoffman I Hamby RI Vectorcardiography 3. North-Holland Publishing Co, Amsterdam1976: 87-95 Google Scholar Study of the high-gain vectorcardiographic P loop can also aid in assessing the site of ectopic supraventricular rhythms with a certain degree of accuracy. 3 Lau SH Cohen SI Stein E et al. P waves and P loops in coronary sinus and left atrial rhythms. Am Heart J. 1970; 79: 201-214 Abstract Full Text PDF PubMed Scopus (26) Google Scholar , 4 Waldo AL Vitikainen KJ Kaiser GA et al. The P wave and P-R interval: Effects of the site of origin of atrial depolarization. Circulation. 1970; 42: 653-671 Crossref PubMed Scopus (69) Google Scholar We describe herein the utility of combined noninvasive techniques in defining the electromechanical sequence of atrial activity in a patient with a distinctly unusual P wave.

Electrophysiologic manifestations in so-called "sick sinus syndrome".

Electrophysiologic disorders in 17 patients with sick sinus syndrome (SSS) were assessed by recording of intracardiac electrograms, atrial overdrive pacing and extrastimulus technique. Significant suppression of the sinoatrial node (SAN) by overdrive pacing (maximum corrected SAN recovery time of longer than 560 msec) was noted in 14 or 16 patients studied. In nine patients, scanning with atrial extrastimuli, sinus rest was defined in all. In one patient there was a longer interpolation zone. Calculated sinoatrial conduction time (SACT) in individual patients varied considerably. The mean SACT was over 110 msec in 5 of 9 patients (56%). Sinus echo was demonstrated in 3; one manifested SAN- re-entrant tachycardia with rates of 72 to 77 beats/min. AV nodal echo was demonstrated in 3, two of them manifested AV nodal re-entrant tachycardia. Intracardiac electrograms revealed prolonged AV conduction time in 2 of 15 patients and prolonged His-Purkinje system conduction time in 2 of 17 patients studied. Two patients disclosed what we thought to be manifestation of intraatrial conduction disturbance. Both had considerable time interval between pacing impulse and atrial response. In one of them Mobitz type 1 and 2:1 intraatrial blocks were observed on atrial pacing and a possible internodal tract depolarization was also recorded. It is concluded that the electrophysiologic manifestations of patients with SSS cover a wide spectrum. The machanism of tachycardia can be due to either SAN or AV nodal re-entry.

A vectorcardiographic study of spatial P, QRS and T-loops in diabetic patients without clinically apparent heart disease

Summary Eighty-nine ambulatory normotensive diabetic patients, free of cardiorespiratory symptoms at any time or any clinical or x-ray evidence of cardiac involvement except for electrocardiographic abnormalities (50.5%), have been studied vectorcardiographically. The abnormalities of the spatial QRS, T and P-loops have been analyzed with regard to the presence of bites, T-loop length/width (L/W) ratio and intra-atrial conduction disturbances. Forty-one percent of patients had QRS bites with a duration more than 10 msec and an amplitude more than 0.1 mV. Thirty-eight percent had an abnormal spatial T-loop L/W ratio of less than 2.6. Twenty-five percent had intra-atrial conduction disturbances. The vectorcardiograms (VCGs) showed 75% of diabetic patients presenting abnormalities of the QRS, T or P-loop (single or combined). These abnormalities may be caused by small and large coronary vessels and myocardial involvement, or they may be due to biochemical changes at the level of the cellular between the duration of the disease, diet or hypoglycemic medication and the vectorcardiographic abnormalities. We concluded that vectorcardiography is a reliable and important non-invasive method for detecting subclinical cardiac abnormalities in patients with diabetes mellitus.