New aspects of the clinical use of anti-arrhythmia agents with special reference to acute therapy of ventricular tachycardia (lidocaine vs. ajmaline)

Antiarrhythmic treatment is based on the hypothesis that ventricular premature beats (VPBs), in the presence of underlying cardiac disease and impaired ventricular function, may predispose to sudden cardiac death. The effectiveness of treatment, however, has not been proven. For acute treatment of paroxysmal ventricular tachycardia, on comparison of the effectiveness of lidocaine and ajmaline, some new aspects have been rendered. VENTRICULAR PREMATURE BEATS (VPB): Isolated VPBs can be found in 40 to 75% of healthy subjects; if their number is substantial, investigation is warranted. For VPBs with subjective symptoms, beta-receptor blockers or specific antiarrhythmic agents, if necessary in combination, may be given. In several studies it has been shown that the prognosis of patients with frequent and complex VPBs, that is couplets and salvos, without heart disease is not compromised. In one long-term study over an average of 6.5 years, sudden death was observed in only one of 70 subjects who had 566 VPBs/24 hours, 60% additionally couplets and 26% salvos in the Holter ECG. Accordingly, treatment for the sake of prognosis is not warranted. For patients with mitral valve prolapse or only mildly impaired ventricular function and asymptomatic arrhythmias, treatment is not necessary since it has not been shown to be beneficial. Coronary artery disease is the most frequent cause of ventricular arrhythmias and sudden death. In numerous studies in patients after myocardial infarction, a relationship has been recognized between frequent and complex VPBs and overall mortality as well as sudden death. Particularly at risk are patients with very frequent and complex VPBs with additional impairment of ejection fraction to less than 30 to 40% but this group only accounts for 10% of patients after infarction. Only in one interventional study, carried out with aprindine, there was a significant reduction in overall mortality from 12.5 to 7.8% with an adverse reaction rate, however, of 21%. In high-risk patients with a low ejection fraction and numerous, complex VPBs as well, in a further study with aprindine, after one year, there was no decrease in overall mortality as compared with the placebo group. The cause for the insufficient effectiveness of the antiarrhythmic agents in various interventional studies has been attributed to a limited number of patients, rigid dosing regimens, inadequate suppression of VPBs and a high incidence of adverse reactions. In the multicenter, randomized, placebo-controlled CAST study with newer substances, a total of 2309 patients with essentially asymptomatic VPBs at a rate of more than 6/hour and an ejection fraction less than 55% or 40% admitted more than 90 days after infarction, respectively, were followed from six days to two years after myocardial infarction to determine if the significant suppression of VPBs in patients with coronary artery disease with antiarrhythmic agents leads to a reduction in arrhythmia-associated deaths. Flecainide, encainide and moricizine led to a significant suppression of VPBs in 75% of the patients. After an average of ten months, the rate of arrhythmia-induced deaths of 4.5% in those treated with encainide or flecainide was significantly higher than the 1.2% observed in the placebo group. These results appear attributable to a proarrhythmic effect of the class IC drugs during long-term treatment.(ABSTRACT TRUNCATED AT 400 WORDS)     

Causes of sudden death in competitive athletes

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.     

Complex ventricular arrhythmias associated with the mitral valve prolapse syndrome. Effectiveness of moricizine (Ethmozine) in patients resistant to conventional antiarrhythmics

On the basis of epidemiologic studies, more than 10 million Americans have echocardiographic evidence of mitral valve prolapse. Although ventricular arrhythmias occur frequently (over 50 percent of patients with mitral valve prolapse), they rarely result in sustained ventricular tachycardia or sudden cardiac death. However, a common problem in clinical practice is a patient with mitral valve prolapse and symptomatic complex ventricular arrhythmias refractory or intolerant to both beta blockers and conventional type I antiarrhythmics. These drugs are known to have frequent side effects, toxicity, and proarrhythmic effects. In 17 patients with mitral valve prolapse who presented with symptomatic complex ventricular arrhythmias and who were unresponsive to an average of the three conventional agents, moricizine (Ethmozine) was effective in suppressing 90 percent of ventricular premature depolarizations, 99 percent of nonsustained runs of ventricular tachycardia, as well as all sustained runs of ventricular tachycardia, resulting in abolition of palpitations, dizziness, and syncopal episodes. Its efficacy as well as its low frequency of minor side effects makes it ideal for future consideration in the population with mitral valve prolapse, who are frequently young and may therefore require therapy for many years.     

The pathology of mitral valve prolapse

The gross criteria for diagnosing prolapsing mitral valve are: 1. interchordal hooding of the involved leaflets, 2. hooding or doming of leaflets towards the left atrium, 3. elongation of the involved leaflets resulting in an increase in valve area, 4. dilatation of the valve annulus in patients with severe mitral regurgitation. The posterior leaflet is most frequently affected. The involved leaflets, in general, are thickened, soft, greyish white and have a smooth atrial surface. Chordae tendineae are described as elongated, tortuous and attenuated or thinned. Deviations from normal chordal insertion have recently been observed which possibly appear to represent the underlying abnormality. Microscopic findings include significant thickening of the spongiosa and the fibrosa, changes in dense collagen fibers in the atrialis layer, occasionally, with fibrin platelet deposits. Histochemical characterization of changes in the spongiosa may also be helpful in the diagnosis. Ultrastructurally, there may be changes in collagen and elastic fibers as well as myxoid areas. On comparison of findings in surgically-removed mitral valves with those of control specimens from autopsy patients with no cardiac abnormalities, the length of the anterior and posterior leaflet as well as the annular ring diameter was larger in the valves with prolapse. Two-dimensional echocardiography accurately assessed leaflet length when compared to morphologic measurements, however, the annular diameter during systole or diastole was smaller. In patients with mitral regurgitation requiring surgery, mitral valve prolapse is the most common cause. Annular ring dilatation and chordae tendineae rupture appear to contribute substantially to incurrence of the mitral regurgitation. The heart weight is increased in the majority of patients with symptomatic mitral valve prolapse but normal, however, in those without symptoms. The most frequent complication of mitral valve prolapse is mitral regurgitation with or without congestive heart failure. Patients with redundant leaflets may be at high risk of sudden death. Young women with abnormal resting ECG, prolonged Q-T interval, family history of sudden death or complex ventricular arrhythmias may also be at a greater risk of sudden death. The incidence of infective endocarditis appears higher in those with redundant than in those with nonredundant valves. The incidence of cerebral ischemic events is low.(ABSTRACT TRUNCATED AT 400 WORDS)     

Mitral valve prolapse syndrome and arrhythmias

In patients with mitral valve prolapse syndrome various disturbances of cardiac rhythm can be observed such as atrial arrhythmias, ventricular tachycardias and conduction disturbances. Of timely interest are the questions of which etiology is at the basis of the arrhythmias, what is their relevance with respect to sudden cardiac death, what are the indications for treatment and which therapeutic results can be anticipated. Cardiac arrhythmias represent the most frequent complication of mitral valve prolapse. Holter ECG monitoring has assumed the central role in detection of all types of arrhythmias. As compared with normal persons, in patients with mitral valve prolapse, both ventricular and supraventricular arrhythmias can be found more frequently. Atrial arrhythmias: Supraventricular arrhythmias can be found less frequently than ventricular arrhythmias (Table 1). Premature atrial contractions can be observed in 35% of those with mitral valve prolapse but also in a similar number of normal individuals such that their presence is not of clinical relevance. There is only a tendency to more frequently incurred supraventricular couplets in mitral valve prolapse. Supraventricular tachycardias can be observed in 10.5 to 32% of which sinus tachycardia (heart rate greater than 120 beats per minute), paroxysmal atrial tachycardia and intermittent atrial fibrillation at about 5 to 6% each are not more common than in control subjects. Atrial fibrillation was seen more frequently in mitral valve prolapse with mitral regurgitation or, conversely, in mitral regurgitation due to mitral valve prolapse more frequently than in mitral regurgitation due to other causes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mitral valve prolapse: definition and implications in athletes

Mitral valve prolapse is probably the most common cardiac valve disorder, affecting approximately 5% of the population. Although it is genetically determined, its clinical manifestations do not usually become evident before adulthood. In the setting of a cardiology referral center, a mitral valve prolapse syndrome, consisting of nonspecific symptoms, repolarization changes on the electrocardiogram and arrhythmias, has been identified. However, doubt has recently been expressed about the existence of such a syndrome. The prognosis of mitral valve prolapse is generally favorable but infrequent complications do occur and include transient ischemic attacks, progression of mitral regurgitation with or without ruptured chordae tendineae, infective endocarditis and sudden death. The symptoms and the complications are not usually related to physical activity. A permissive attitude toward participation of patients with mitral valve prolapse in competitive athletics is probably warranted; however, it would appear reasonable to disqualify athletes with mitral valve prolapse in the following circumstances: history of syncope; disabling chest pain; complex ventricular arrhythmias, particularly if induced or worsened by exercise; significant mitral regurgitation; prolonged QT interval; Marfan's syndrome; and family history of sudden death.     

Ventricular extrasystole: prognostic value and therapeutic indication

Ventricular beats are abnormal rhythms which are frequently detected by modern recording techniques in healthy subjects as well as in patients with heart disease. In the first case, analysis of the literature enables us to exclude any pejorative prognostic implication associated with V.E.B., in the absence of any major risk factor for coronary artery disease. However, when there is an underlying heart disease, a number of subgroups can be distinguished with a high risk of sudden death: coronary insufficiency associated with ischaemic cardiomyopathy, especially in the early post-hospital phase after a myocardial infarction; hypertrophic cardiomyopathy with ventricular tachycardia on the Holter monitor, family history of sudden death, personal past history of syncope; mitral prolapse with clinical symptoms and auscultatory signs; idiopathic long QT syndrome. In contrast, V.E.B.s do not appear to have prognostic significance in idiopathic hypokinetic cardiomyopathies and aortic valvular disease. In general, it is more the clinical setting than the actual morphology which determines the prognostic implications of ventricular extrasystoles. The sub-groups at high risk should be treated with anti-arrhythmics, but the evaluation of the effectiveness of such treatment remains uncertain and the authors believe that the development of studies of ventricular stimulation prior to and during treatment are justified.     

Ventricular fibrillation in a patient with 'silent' mitral valve prolapse

A patient with clinically silent mitral valve prolapse experienced an episode of out-of-hospital cardiac arrest due to ventricular fibrillation. This arrhythmia was easily replicated in the electrophysiology laboratory and despite treatment with amiodarone alone and amiodarone in combination with propranolol. Amiodarone in combination with quinidine prevented the induction of ventricular fibrillation and proved effective during a 3-year follow-up period. Even though a clear-cut relationship between the arrhythmias and mitral valve prolapse cannot be established, this case suggests that sudden death can occur in patients with mitral valve prolapse but without the known risk factors for the development of sudden death.     

Risk factors for sudden death after acute myocardial infarction: two-year follow-up

The risk of sudden coronary death after myocardial infarction (MI) was assessed in 533 patients who survived 10 days after MI and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of multiple clinical and laboratory variables determined before hospital discharge revealed that frequent ventricular premature beats (VPBs) (greater than or equal to 10/hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction less than or equal to 0.40) were independently significant markers of risk for subsequent sudden death believed to be the result of a primary ventricular arrhythmia. The incidence of sudden death was 18% in patients with both LV dysfunction and frequent VPBs (11 times that of patients with neither of these findings). Seventy-nine percent of all sudden deaths occurred within 7 months after the index MI. In 280 survivors reclassified 6 months after MI with regard to the presence or absence of frequent VPBs and LV dysfunction, these risk factors could not be associated with sudden coronary death over a further follow-up period of up to 18 months; the overall incidence of sudden cardiac death was low (1.4%) after 6 months. Thus, the presence of frequent VPBs in association with LV dysfunction early after MI identifies patients at high risk for sudden death over the next 7 months.     

Sudden cardiac death caused by native aortic valve thrombosis in an adult patient with a complex congenital cyanotic heart disease

Cyanotic congenital heart disease is associated with an increased risk of thromboembolism. We describe the case of sudden cardiac death caused by native aortic valve thrombosis in adult cyanotic patient. Such embolic complication was not previously described in cyanotic patient. It is also the first report of sudden cardiac death as an initial presentation of the native aortic valve thrombosis. Cyanotic congenital heart disease (CCHD) is associated with an increased risk of thromboembolism due to different haemathologic abnormalities associated with hypoxemia and secondary polycythemia [H. Kajimoto, M. Nakazawa, K. Murasaki, et al. Increased thrombogenesity in patients with cyanotic congenital heart disease. Circ J Jun 2007;71(6):948-953]. Cerebrovascular events, venous and arterial thrombosis have been described in patients with CCHD [N. Ammash, C.A. Warnes. Cerebrovascular events in adult patients with cyanotic congenital heart disease. J Am Coll Cardiol Sep 1996;28(3):768-772]. We present a case of the native aortic valve thrombosis in an adult patient with a complex cyanotic congenital heart lesion which led to sudden death.     

Cardiac function during rest and exercise in patients with mitral valve prolapse: Role of radionuclear angiocardiography

The clinical features of mitral valve prolapse syndrome and ischemic coronary disease overlap, making differentiation of the two conditions difficult. Furthermore, many patients have both conditions. This study assessed changes in ventricular function during rest and exercise in patients with mitral valve prolapse alone and in patients with prolapse and concomitant coronary artery disease. Twelve patients with angiographically documented mitral valve prolapse and normal coronary anatomy and 11 patients with normal coronary anatomy and no mitral valve prolapse had increased ejection fraction and demonstrated no wall motion abnormality during exercise. Changes in ventricular function during exercise in 11 additional patients with mitral valve prolapse demonstrated on echocardiography were similar to those in the group with mitral valve prolapse and normal coronary anatomy seen on angiography. In contrast, 6 of 11 patients with mitral valve prolapse and coronary arterial stenosis demonstrated on angiography had a decreased ejection fraction and exhibited wall motion abnormalities during exercise. These results suggest that mitral valve prolapse alone has no detrimental effect on ventricular function during rest and exercise and that exercise-induced abnormalities in ventricular function are related to the presence and severity of coronary artery disease and not to mitral valve prolapse.     

Mitral valve prolapse due to coronary artery disease

Controversy exists concerning the etiologic role of coronary artery disease in the prolapsing mitral valve leaflet syndrome. A 35 year old man with progressive coronary artery disease is described. Auscultation before and after his first myocardial infarction revealed only a fourth heart sound; subsequent left ventricular cineangiography demonstrated normal anatomy and function of the mitral valve, despite extensive wall motion abnormalities. Six months later he experienced another myocardial infarction after which the typical mid-systolic click, late systolic murmur of mitral valve prolapse developed. A second left ventricular cineanglogram at this time revealed mid-systolic mitral valve prolapse and mitral regurgitation. This patient's course indicates that myocardial damage from coronary artery disease can cause mitral valve prolapse in patients without preexisting redundant mitral valve tissue.     

Mitral valve prolapse

Mitral valve prolapse has previously been found to be associated with severe cardiovascular complications such as embolic insults, infectious endocarditis, and sudden cardiac death. However, at the same time, in particular after adopting M-mode and 2D echo for diagnosis, prevalence of the disease was found to be very high, especially in the young. The dilemma of a disease which is frequent and mostly asymptomatic, but in some cases has catastrophic complications, has been solved by implementation of more restrictive diagnostic criteria based on an appreciation of the spatial morphology of the mitral annulus. These criteria call for diagnosis exclusively based on long axis views and a prolapse of > 2 mm beyond a line connecting the leaflet insertion points. "Classic prolapse" additionally requires diastolic thickness of the mitral leaflets of at least 5 mm. Two recent studies, a population-based study of mitral valve prolapse prevalence, and a case-control study of juvenile stroke patients compared to a group of young patients without a history of stroke, shed further light on this disease. The authors found that prevalence of mitral valve prolapse in an average population is 2-3% (1.3% for classic prolapse), without age or sex preponderance; the rate of cerebrovascular insults, congestive heart failure, and atrial fibrillation of patients with prolapse does not exceed that of the rest of the population; however, mitral insufficiency is more frequent; young patients with a history of cerebrovascular insult do not have higher mitral valve prolapse rates than young patients without previous insult.     

Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations.

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.     

Late potentials in patients with prolapse of the mitral valve]

Recently published reports have highlighted the presence of a high incidence of late potentials in patients with mitral valve prolapse. In order to verify this observation 29 patients suffering from this pathology were studied using high-resolution electrocardiography. Late potentials were present in 24% of patients with mitral valve prolapse in comparison to 5% of control subjects (p less than 0.05); no correlation was found however in patients with mitral valve prolapse between the presence of late potentials and Holter's ventricular hyperkinetic tachycardia. At a follow-up after 16 +/- 4 months no patient presented persistent ventricular tachycardia or sudden death. The presence of late potentials might be yet symptom of the mitral prolapse syndrome whose prognostic role, although not yet clear, does not appear to represent a negative factor in relation to major tachycardia attacks.     

Complications of idiopathic mitral valve prolapse. Prevention and treatment

Mitral valve prolapse is the most common form of heart disease, as it occurs in 4 to 6 per cent of the population. It has a benign course in the majority of cases, but 5 types of severe complication can occur in 15 per cent of cases. Mitral incompetence occurs in 14.8 per cent of cases. It may develop gradually or suddenly, following rupture of the chordae, which requires rapid surgical repair. Mitral valve prolapse is complicated by infectious endocarditis in 2.9 per cent of cases, hence the need for antibiotic prophylaxis prior to dental treatment or surgery in patients with a pan-systolic or end-systolic murmur. The only arrhythmias which should be considered as complications and treated as such are frequent ventricular extrasystoles of more than 30 per hour, usually associated with bigeminy, runs or polymorphism, ventricular tachycardia and ventricular fibrillation. Treatment consists, primarily, of beta-blockers. Sudden death is of course the major complication, occurring in 1.4 to 2.4 per cent of cases. The patients at risk of this complication are middle-aged women (40 years) with a past history of syncope or faintness due, in most cases, to episodes of ventricular tachycardia or ventricular fibrillation. Apart from arrhythmia, coronary artery spasm has also been found to be a cause of sudden death in these patients. Transient or definitive ocular and cerebral ischaemic episodes can also complicate mitral valve prolapse. Mitral valve prolapse is found in 20 to 30 per cent of patients with neurological accidents before the age of 45. Preventative treatment consists of anti-platelet aggregation agents and anticoagulants in recurrent cases.     

Ventricular premature beats on Holter monitoring in patients admitted with chest pain, in whom acute myocardial infarction is not confirmed. The prognostic value and relationship to scars or ischemia on thallium-201 scintigraphy

Ambulatory 24-h Holter monitoring was carried out in 198 patients who had been admitted because of suspected acute myocardial infarction (AMI) due to chest pain, but in whom AMI was not confirmed. During a follow-up period of 12-24 months (median 14 months) 16 cardiac events (i.e., nonfatal AMI or cardiac death) occurred. Ventricular premature beats (VPBs) were found in 65.2% of the patients, complex VPBs in 28.8%. Pairs of VPBs which were seen in 10.0% of the patients were the only important type of VPBs significantly related to an impaired prognosis. Thallium-201 scintigraphy was performed in 144 of the patients. VPBs were significantly related to scar formation (i.e., to permanent defects, but not to ischemia, specifically, to transient defects). It is concluded that ventricular arrhythmias in this patient category indicate presence of chronic ischemic heart disease, and that pairs of VPBs seem to identify patients at risk for cardiac events.     

Mitralklappenprolaps: Identifikation von Patienten mit erhöhtem Risiko und therapeutisches Management

Mitral valve prolapse shows a wide spectrum from a benign anatomic variant to a progressive disease with severe cardiovascular morbidity and mortality. Echocardiography is the most important tool for diagnosis and risk stratification. Predictors for high risk are significant thickening of mitral leaflet of > 5 mm ("classic" prolapse), moderate to severe mitral regurgitation and reduced left ventricular function. These patients have an increased risk of infective endocarditis, cerebral ischemia and sudden cardiac death. Because of the risk for the development of severe mitral regurgitation requiring surgery short follow-up intervals are necessary.In mitral prolapse syndrome cardiac clinical signs (palpitation, rhythm disorders, syncope, etc.) are associated with a prolapse that can be treated symptomatically with drugs after exclusion of other causes and significant mitral regurgitation requiring surgery.     

Angiographic diagnosis of mitral valve prolapse: Correlation with echocardiography

Mitral valve prolapse is characterized clinically by a nonejection systolic click and a late systolic murmur and angiographically by end-systolic bulging of one or both mitral leaflets into the left atrium. If one accepts the end-systolic configuration of the left ventriculogram as the diagnostic standard, recent studies suggest that mitral valve prolapse may frequently be associated with certain other forms of cardiac disease. To determine the incidence of this finding in patients unselected for their primary cardiac diagnosis, the left ventricular angiograms from 336 consecutive patients (223 men and 133 women) were analyzed. Six patients had the clinical diagnosis of click-murmur syndrome, and all six had angiographic prolapse. Leaflet bulging was also present in 52 of 131 patients with ischemic heart disease (40 percent), 27 of 84 with rheumatic valve disease (32 percent), 3 of 19 with cardiomyopathy (16 percent), 5 of 12 with congenital heart disease (42 percent) and 50 of 84 with chest pain and no significant coronary artery disease (60 percent). Technically satisfactory echocardiograms were available from 140 of these patients; mitral valve prolapse was evident in the echocardiograms of 9 (6.4 percent), including 6 with the click-murmur syndrome.     

Etiology and pathogenesis of thromboembolism.

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.