Ventricular Mural Thrombosis Research Articles

Dilated Cardiomyopathy in Children: Early Detection and Treatment.

Cardiomyopathy is segregated into primary and secondary categories, leading to different phenotypes, including dilated, hypertrophic, and restrictive patterns. Dilated cardiomyopathy (DCM) is a mixed bag of heart diseases with the unique features of cardiac dilatation and subnormal to poor myocardial contractility. Dilated cardiomyopathy in the pediatric age group is generally characterized by unobstructed, dilated, and contracting left ventricular chamber defects and is associated with heart failure. Other causes include genetic juvenile-onset cardiomyopathy, drug-induced cardiomyopathy, stress-induced cardiomyopathy, hemochromatosis, endocrine causes (thyroid disorder and pheochromocytoma), autoimmune diseases, and nutritional deficiencies (selenium and thiamine). It is characterized by thinning of the left ventricle, a dilated left ventricle or biventricular dilatation, left ventricular systolic dysfunction, left ventricular diastolic dysfunction, global hypokinesia, and cardiomegaly (seen on a chest X-ray). Decreased cardiac output leads to fatigue, cachexia, narrow pulse pressure, dicrotic pulse/hypokinetic pulse, dyspnea, cool extremities, decreased blood supply to the brain (cognitive dysfunction), and reduced blood supply to the kidney (renal failure). Left ventricular diastolic dysfunction can result in dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Cardiomyopathy can also occur with or without left ventricular dysfunction, as in left ventricular non-compaction cardiomyopathy (LVNC), which is a rare heart disease occurring due to two (likely) pathogenic nonsense mutations: DSG2-p.S363X and TBX20-p.D278X. The study of familial forms of LVNC is helpful for risk prediction and genetic counseling of relatives. Right ventricular chamber failure can be identified on the electrocardiogram as sinus tachycardia and non-specific ST/T changes. The complications include arrhythmia (atrial fibrillation) and thromboembolism (left ventricular mural thrombosis). It is of utmost importance in the field of heart transplantation as the definitive treatment of the disease. Heart transplantation is now an acceptable treatment option for patients with dilated cardiomyopathy. This short review highlights different methods for the detection and diagnosis of dilated cardiomyopathy and the treatment modalities available for the same.

Right ventricular mural thrombus formation superimposed on previous anterior myocardial infarction

In the differential diagnosis of the occurrence of right ventricular mural thrombosis after apparent resolution of an episode of anterior myocardial infarction [ [1] Wei F. Fangang W. Jiangli H. Zhaoping L. Lijun G. Wei G. Recurrent intraventricular thrombus following myocardial infarction. Int. J. Cardiol. 2015; 181: 315-316 Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar ], there should be a high index of suspicion for the occurrence of new-onset silent inferior myocardial infarction as the underlying cause of new onset right ventricular thrombus formation [ [2] Ahdout D.J. Damani P.M. Ultan L.B. Recurrent acute pulmonary emboli in association with acute myocardial infarction. Chest. 1989; 96: 682-684 Crossref PubMed Scopus (8) Google Scholar ], and an equally high index of suspicion that right ventricular thrombus formation might, in turn, be complicated by the occurrence of pulmonary embolism (PE) [ [2] Ahdout D.J. Damani P.M. Ultan L.B. Recurrent acute pulmonary emboli in association with acute myocardial infarction. Chest. 1989; 96: 682-684 Crossref PubMed Scopus (8) Google Scholar ]. The superimposition of the burden of inferior myocardial infarction on the pre-existing burden of anterior myocardial infarction would account for the reported deterioration in left ventricular systolic function, with resulting symptomatic congestive heart failure [ [1] Wei F. Fangang W. Jiangli H. Zhaoping L. Lijun G. Wei G. Recurrent intraventricular thrombus following myocardial infarction. Int. J. Cardiol. 2015; 181: 315-316 Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar ].

Pulmonary Thromboembolism Following Splenectomy in Hereditary Spherocytosis

Hereditary spherocytosis is an inherited disorder characterized by presence of spherocytes. It usually manifests clinically as triad of anaemia, splenomegaly and jaundice. The recommended treatment in a symptomatic patient is splenectomy. Occurrence of pulmonary thromboembolism in hereditary spherocytosis following splenectomy is unusual. We report the case of a 30 year old male who underwent splenectomy for hereditary spherocytosis and subsequently developed pulmonary thromboembolism and right ventricular mural thrombosis six years later. His showed no other procoagulant disorders. The development of pulmonary thromboembolism and right ventricular mural thrombosis in a patient of hereditary spherocytosis after splenectomy is an interesting association. doi:10.4021/jmc2010.06.102e

Pulmonary Thromboembolism Following Splenectomy in Hereditary Spherocytosis

Hereditary spherocytosis is an inherited disorder characterized by presence of spherocytes. It usually manifests clinically as triad of anaemia, splenomegaly and jaundice. The recommended treatment in a symptomatic patient is splenectomy. Occurrence of pulmonary thromboembolism in hereditary spherocytosis following splenectomy is unusual. We report the case of a 30-year-old male who underwent splenectomy for hereditary spherocytosis and subsequently developed pulmonary thromboembolism and right ventricular mural thrombosis six years later. His showed no other procoagulant disorders. The development of pulmonary thromboembolism and right ventricular mural thrombosis in a patient of hereditary spherocytosis after splenectomy is an interesting association. J Med Cases. 2010;1(1):14-15 doi: https://doi.org/10.4021/jmc2010.06.102e

American Heart Association Prevention Conference. IV. Prevention and Rehabilitation of Stroke. Etiology of stroke.

The diagnosis of arterial stroke differentiates ischemia from hemorrhage. The former may be due to arterial occlusion or stenosis, the latter to leakage or rupture of an artery. Computed tomography (CT) and magnetic resonance imaging (MRI) have shown that this basic differentiation cannot be reliably made from the history and clinical examination alone. Of the clinical stroke syndromes, only Wallenberg’s syndrome has not been reported to be due to hemorrhage. When CT or MRI is not available for diagnosis, spinal tap is reliably positive only when the aneurysm or arteriovenous malformation has ruptured into the subarachnoid space; the results are often normal when a small hemorrhage occurs in the parenchyma. For some therapies, notably neuroprotective agents, the potential benefits for ischemia do not seem to be offset by potential harm in the case of hemorrhage. However, because fibrinolytics, antithrombotic agents, or surgery are treatment options, diagnostic certainty is essential to avoid harming the patient. Most—but not all—strokes have a sudden or rapidly evolving onset. Differential diagnosis of sudden change in focal neurological status includes seizures or postepileptic paralysis, hemorrhage into a tumor (itself a form of stroke), and migraine. Neuroimaging helps to differentiate between these and the cause of short-lived symptoms (transient ischemic attack [TIA]) usually presumed due to ischemia but possibly due to new-onset infarction or hemorrhage. More precise classification of stroke into a pathogenic subtype (embolism, thrombosis, decreased perfusion or “lacunar” infarction, leakage, or rupture) evades the best clinical skills. The classification of stroke mechanism depends on the presence of risk factors for stroke (preexisting condition or circumstance epidemiologically related to stroke) and etiologies (disease directly causing the mechanism) that implicate the cause of stroke in a given patient. However, more than one risk factor and etiology are frequently present in the same patient and may be related …

Pathogenesis of Low Output in Right Ventricular Myocardial Infarction

Although left ventricular dysfunction is the most frequent cause of decreased cardiac output, impaired right ventricular function may also produce low output syndrome. Right ventricular dysfunction can be observed in a number of clinical conditions: right ventricular infarction, acute massive pulmonary embolism, severe primary tricuspid and pulmonary regurgitation, dilated cardiomyopathy, chronic right ventricular outflow obstruction, chronic pre- and postcapillary pulmonary hypertension, congenital right ventricular dysplasia, and infiltrative diseases involving the right ventricle. Of all of these various clinical pathophysiologic disorders, acute right ventricular myocardial infarction is probably the most frequent clinical condition that has the potential to precipitate acute low-output state. Although isolated right ventricular infarction is uncommon, the right ventricle is frequendy involved in patients in whom left ventricular infarction develops. The involvement of the free wall of the right ventricle is frequently seen in patients with left ventricular inferior or inferoposterior wall myocardial infarction. Based on the diagnostic criteria, right ventricular myocardial infarction is observed in up to 40 percent of patients with left ventricular inferior wall myocardial infarction. 1 Sharpe DN Botvinick EH Shames DM et al. The noninvasive diagnosis of right ventricular infarction.. Circulation. 1978; 57: 483-490 Crossref PubMed Scopus (152) Google Scholar The clinical right ventricular myocardial infarction is infrequently observed in patients with left ventricular anterior wall myocardial infarction. A number of complications can be encountered in patients with predominant right ventricular myocardial infarction, although the incidence is comparatively low. Bradyarrhythmias, including sinus bradycardia, sinus arrest, sinoatrial exit block, and various degrees of atrioventricular block are more frequent in patients with right ventricular infarction compared with patients with left ventricular infarction. Right ventricular infarction results most frequently from thrombotic occlusion of the right coronary artery that also provides blood flow via atrioventricular (AV) nodal artery to the AV node in over 90 percent of instances. Thus, AV nodal ischemia and varying degrees of AV nodal block frequendy accompany right ventricular infarction. Occlusion of the right coronary artery, proximal to the origin of the sinoatrial nodal artery, may also produce sinus nodal dysfunction and right ventricular myocardial infarction. Besides bradyarrhythmias, right ventricular myocardial infarction can also produce hypotension and low-output state. The incidence of severe low-output state with clinical features of cardiogenic shock occur in approximately 10 percent of patients with right ventricular infarction. The other complications, such as free wall rupture with or without ventricular septal rupture, pulmonary embolism associated with right ventricular mural thrombosis, and severe tricuspid regurgitation resulting from right ventricular papillary muscle infarction are very infrequently encountered.

Heparin therapy. Regimens and treatment considerations.

Heparin is a parenteral antithrombotic agent with efficacy in the treatment and prevention of venous thromboembolic disease and in preinfarctional angina. Accumulating evidence also suggests that heparin is useful in the prevention of coronary artery reocclusion after thrombolytic therapy for acute myocardial infarction, and in the prevention of left ventricular mural thrombosis after anterior wall myocardial infarction. Heparin appears to offer only marginal benefit in reducing mortality when given in combination with thrombolytic therapy and aspirin for acute myocardial infarction. When used for prevention of venous thromboembolism in moderate risk patients, heparin should be given subcutaneously in a dose of 5000 U every 12 hours for 5 to 7 days or until the patient is ambulatory. In higher risk patients, such as those undergoing total hip replacement, heparin should be given subcutaneously every 12 hours in a dose to prolong the activated partial thromboplastin time (aPTT) by 4 to 5 seconds into the upper normal range. When used to treat active venous thromboembolism or the peri-infarctional state, heparin should be given by intravenous infusion with loading and maintenance doses to consistently prolong the aPTT to between 1.5- and 2.5-fold the control value (mean of laboratory's normal range). If constant intravenous infusion is not possible, the drug should be given subcutaneously every 12 hours to consistently prolong the aPTT between 1.5 and 2.5 times control. This regimen is also recommended in pregnant women with venous thromboembolic disease or mechanical heart valves.

An Overview of Therapeutic Interventions in Myocardial Infarction

The high risk of subsequent mortality and morbidity following the occurrence of a myocardial infarction (MI) underlies the importance of instituting effective preventive regimens as part of the overall management of these patients. The aim of such treatment is to prolong survival by preventing sudden and non-sudden death and further major cardiovascular events. Currently available data from randomised, controlled clinical trials in MI patients indicate that early treatment with thrombolytic agents [streptokinase, anisolyated plasminogen streptokinase activator complex (APSAC) or recombinant tissue-type plasminogen activator (rt-PA)] in the first few hours after onset of symptoms significantly reduces the short term mortality following MI, with follow-up studies at 1 year indicating that the early benefits persist long term. The optimum time for initiation of thrombolytic therapy is within 6 hours of onset, but treatment started between 7 and 24 hours after onset can also be beneficial. Similarly, there is good evidence that beta-blockers (e.g. propranolol, timolol, metoprolol, atenolol) and aspirin are effective in reducing both the mortality and reinfarction rate following MI. With beta-blockers, a policy of starting treatment early intravenously and continuing orally for 2 to 3 years seems likely to save more lives than either strategy alone; however, contraindications to beta-blockade reduce the number of patients eligible to receive this treatment. In the case of aspirin, the optimum dosage has yet to be determined, but on the basis of present evidence, it seems reasonable to start treatment early with doses of 160 to 325 mg daily and continue for a year or 2 after recovery. Other studies have shown that long term oral anticoagulant therapy is also effective in reducing the mortality and reinfarction rate after MI. Subcutaneous heparin therapy given for 10 days in patients with acute anterior MI reduces the frequency of left ventricular mural thrombosis, while intravenous heparin given for greater than or equal to 4 days improves coronary artery patency rates following administration of a thrombolytic agent. In a comparison with low dose aspirin, intravenous heparin proved more effective in maintaining coronary artery patency rates after rt-PA thrombolysis. There is also evidence that oral nitrates may reduce mortality in MI patients, especially in those with heart failure. However, current data on the use of antiarrhythmic drugs do not support the routine of these drugs following MI. Similarly, with lipid-lowering agents, the evidence that lowering cholesterol is beneficial in reducing mortality after MI is at present inconclusive. Further studies with these groups of drugs are awaited with interest.(ABSTRACT TRUNCATED AT 400 WORDS)

High dose heparin reduces the incidence of left ventricular mural thrombosis

High dose heparin reduces the incidence of left ventricular mural thrombosis

Prevention of left ventricular mural thrombosis and arterial embolism during and after acute myocardial infarction

Prevention of left ventricular mural thrombosis and arterial embolism during and after acute myocardial infarction

New approaches to treatment of myocardial infarction

Survival of patients with acute transmural infarction is largely related to the size of the myocardial infarction. The goal of thrombolytic therapy in acute myocardial infarction is maximal salvage of myocardium by reestablishment of flow in the occluded infarct-related artery and the establishment and maintenance of a patent infarct-related artery. Results of randomized trials show a significant reduction in mortality in patients who have undergone thrombolysis. A patent infarct-related artery, even in the absence of a change in left ventricular function, is associated with reduced mortality. The Thrombolysis in Myocardial Infarction Trial and the European Cooperative Trial showed that recombiant tissue-type plasminogen activator is superior to streptokinase in reestablishing flow in a totally occluded artery. Experimental and clinical evidence suggests that thrombolysis and thrombosis occur simultaneously, and that lysis appears to increase both thrombin and platelet activity. Effective reduction of thrombosis accelerates thrombolysis. Rethrombosis after thrombolysis is due to anchored residual thrombus, which alters the hemorrheology of blood flow and produces a highly thrombogenic substrate that is largely due to residual fibrin-bound thrombin. Platelet deposition is directly related to severity of residual stenosis and shear rate. Thrombin appears to be the most potent of the 5 potential stimulators of platelet activation during arterial thrombosis. Proper anticoagulation can play an important role in reducing thrombosis. Experimental evidence strongly supports the use of heparin during and after thrombolysis. A recently reported study shows continued reduction of residal stenosis after 1 month of vigorous anticoagulation with intravenous heparin and subsequent oral anticoagulation. A recent clinical trial showed that subcutaneous heparin given during hospitalization reduced recurrent ischemia after thrombolysis, mortality and left ventricular mural thrombosis. Most current trials are using both heparin and aspirin during and after thrombolysis, with apparent reduction in rates of reocclusion. Thrombolysis with a combination of recombinant tissue-type plasminogen activator and either streptokinase or urokinase appears to reduce reocclusion. Maximal therapy to enhance continued lysis of residual mural thrombus after hospitalization includes combined anticoagulation with sodium warfarin and probably low-dose aspirin at 80 mg/day.

Anticoagulant therapy after acute myocardial infarction

The use of anticoagulant therapy for patients who have had an acute myocardial infarction is still controversial, mainly because early major studies had conflicting findings, but reanalysis of the data did produce evidence that anticoagulation had clinically and statistically significant benefits. Now more evidence, including the results of a 10-day in-hospital study of low- and high-dose calcium heparin, has been gathered to support using anticoagulants for these patients. The study used the development of left ventricular mural thrombosis, a frequent complication of acute myocardial infarction that carries a high risk for systmic embolic complications, to assess clinical outcome: A reduced incidence of mural thrombosis would be taken to indicate reduced chances that patients would have major systemic emboli. Two-dimensional echocardiography was used to detect thrombi. In the study, the incidence of left ventricular mural thrombosis was significantly lower in the high-than in the tow-dose group. Among patients in the high-dose group in whom a mural thrombosis did develop, plasma heparin concentrations were significantly lower and activated partial thromboplastin times were shorter. These data suggest that monitoring plasma heparin levels and anticoagulant response can ensure maximal treatment effectiveness. No significant differences in other outcomes—such as bleeding complications, nonhemorrhagic strokes and mortality—were found between the high- and tow-dose treatment groups.

Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction : Turpie AGG, Robinson JG, Doyle DJ, et al N Engl J Med 320:352–357, 1989

Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction : Turpie AGG, Robinson JG, Doyle DJ, et al N Engl J Med 320:352–357, 1989

Prevention of left ventricular mural thrombus

Acute myocardial infarction is associated with a high incidence of left ventricular mural thrombosis, which causes most of the systemic emboli. A double-blind trial was undertaken in patients with anterior transmural myocardial infarction to evaluate the ability of a high-dose heparin regimen to prevent left ventricular mural thrombosis. The high dose consisted of 12,500 U of calcium heparin subcutaneously every 12 hours for 10 days, which was compared with a low dose consisting of 5,000 U every 12 hours. The formation of left ventricular mural thrombosis was assessed by means of 2-dimensional echocardiography on day 10 after infarction. The high-dose group had a significantly lower incidence of left ventricular mural thrombosis than did the low-dose group. This was achieved without increasing the incidence of bleeding. The benefits of high-dose heparin were associated with maintaining plasma heparin concentrations at 0.2 U/ml and activated partial thromboplastin time between 50 and 60 seconds.

RANDOMISED CONTROLLED TRIAL OF SUBCUTANEOUS CALCIUM-HEPARIN IN ACUTE MYOCARDIAL INFARCTION: THE SCATI (STUDIO SULLA CALCIPARINA NELL'ANGINA E NELLA TROMBOSI VENTRICOLARE NELL'INFARTO) GROUP

In a multicentre study 711 patients were randomised to a group receiving calcium-heparin, 12 500 U, subcutaneously (360), or to a group receiving no heparin (351), beginning within 24 h of the onset of symptoms. 433 of these patients, admitted within 6 h, were given intravenous streptokinase (SK). Results were analysed for the in-hospital period. Calcium-heparin had no significant effects on the frequency of electrocardiographically documented ischaemic episodes or non-fatal reinfarction in the whole series; in the subgroup receiving SK, transient ischaemic episodes recurred in 14·2% of those treated with heparin vs 19·6% of the controls (p = 0·08). Mortality was significantly lower in the calcium-heparin treated patients, both in the overall groups (21/360 vs 35/351, p=0·03) and in the SK subgroups (10/218 vs 19/215, p=0·05). In 200 patients with first anterior myocardial infarction, it was possible to assess the effect of heparin on left ventricular mural thrombosis. On predischarge two-dimensional echocardiography, the prevalence of thrombus was significantly lower in the heparin group than in the control group (19/107 vs 34/93). Heparin also greatly reduced the incidence of thrombus formation in those who were thrombus-free on admission. Complications of heparin treatment were few.

Antithrombotic therapy in acute myocardial infarction: Prevention of venous, left ventricular and coronary artery thromboembolism

The antithrombotic approach to patients with acute myocardial infarction in the prevention of venous, left ventricular and coronary artery thromboembolic events should be based on an understanding of pathogenesis and risk. Coronary thrombotic events involve conditions of high shear rate present in areas of vessel stenosis or disrupted atherosclerotic plaque, which lead to activation of both platelets and the coagulation system, and are best prevented by platelet inhibitors alone or in combination with an anticoagulant. However, thromboembolism that originates in the venous system or cardiac chambers is related to situations of blood stasis and low shear rate, which predominantly result in clotting activation and fibrin-thrombus formation and are best approached with anticoagulant therapy. For prevention of venous thrombosis and pulmonary embolism, early mobilization is essential and should be supplemented by low-dose heparin in patients at high risk, including the elderly and those with large infarcts, heart failure or previous thromboembolic events. For prevention of left ventricular mural thrombosis and systemic embolism, high-dose heparinization is indicated in patients with large infarcts, particularly in the anterior location and in those with heart failure. Subsequently, warfarin therapy should be considered for patients at high embolic risk, including those with echocardiographic evidence of mobile and protruding thrombi, severe left ventricular dysfunction or prior emboli. In patients with acute infarction, aspirin is recommended for preventing coronary reocclusion and reinfarction. Although anticoagulants may also be of benefit for this purpose, their use is still controversial.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of High-Dose with Low-Dose Subcutaneous Heparin to Prevent Left Ventricular Mural Thrombosis in Patients with Acute Transmural Anterior Myocardial Infarction

We performed a double-blind randomized trial comparing high doses of subcutaneous heparin (12,500 units every 12 hours) with low doses (5000 units every 12 hours) for 10 days in the prevention of left ventricular mural thrombosis in 221 patients with acute anterior myocardial infarction. Left ventricular mural thrombosis was observed by two-dimensional echocardiography on the 10th day after infarction in 10 of 95 patients (11 percent) in the high-dose group and in 28 of 88 patients (32 percent) in the low-dose group (P = 0.0004). One patient in the high-dose group and four in the low-dose group had nonhemorrhagic strokes (P = 0.17). One patient in the low-dose group had a fatal pulmonary embolism. There was no difference in the frequency of hemorrhagic complications, which occurred in six patients in the high-dose group and four in the low-dose group. The mean (+/- SEM) plasma heparin concentration was 0.18 +/- 0.017 U per milliliter in the high-dose group and 0.01 +/- 0.005 U per milliliter in the low-dose group (P less than 0.0001). In the high-dose group, the mean plasma heparin concentration was 0.10 +/- 0.029 U per milliliter among patients with abnormal two-dimensional echocardiograms, as compared with 0.19 +/- 0.019 U per milliliter among patients with normal echocardiograms (P = 0.01). We conclude that heparin administered subcutaneously in a dosage of 12,500 units every 12 hours to patients with acute anterior transmural myocardial infarction is more effective than a lower dosage (5000 units every 12 hours) in preventing left ventricular mural thrombosis.

Incidence of systemic thromboembolic lesions in acute myocardial infarction.

In a series of 1277 cases of acute myocardial infarction, 30 episodes of systemic, noncerebral, thromboembolic lesions in 22 patients have been detected. Locations most frequently involved were the extremities (60%), kidneys (16.6%), spleen (13.3%), and mesentery (10%). The incidence of thromboembolism has been higher in patients over the age of 60. In the great majority of cases, the myocardial infarction has been anterolateral, often with a superimposed pump failure. Mortality has been very high (54.5%), perhaps in relation to the advanced age of the patients and to the extension of the infarction. Embolism at the extremities has been well treated with Fogarty's catheter. Among patients whose postmortem examination has been performed a high incidence of ventricular aneurysm (3 of 7) and mural thrombosis (5 of 7) has resulted. In the cases of ventricular aneurysm, episodes of atrial fibrillation have always occurred.

Primary Mural and Venous Thrombosis in the Heart*

SummaryTen cases are presented of ventricular mural thrombosis and thebesian vein thrombosis with an adequate coronary system and without myocardial necrosis or myocarditis. In six cases there was reason to suspect a thrombosing tendency : namely, extensive neoplastic disease in four cases, thrombophlebitis in one, and small bowel infarction in one.