Myocardial Involvement In Patients Research Articles

Mycobacterium avium-intracellulare Pericardial Effusion

The development of new management techniques for human immunodeficiency virus (HIV) allows for longer latency and survival times. Cardiac complications, including pericardial effusion, are being recognized more frequently [1]. Myocardial involvement in patients with Mycobacterium avium-intracellulare (MAI) is documented [2], but MAI as a cause of pericardial effusion in patients with HIV is described in only a few published cases [3–8]. We present a case that highlights the natural course of an untreated MAI infected pericardial effusion and briefly review the literature on this subject. Case Report. A 29-year-old HIVinfected man (Centers for Disease Control and Prevention stage C3) presented to our hospital with a 3-month history of fever, cough, and dyspnea on exertion. The patient had a long history of noncompliance with his antiretroviral therapy. He had received various combinations of the following medications in the years before admission: zidovudine, didanosine, zalcitabine, and ritonavir. He had not been taking antiretrovirals for an undetermined amount of time at presentation. His CD4 lymphocyte count was 27/mm 3 . The patient’s HIV RNA viral load was elevated. Physical examination revealed resting tachycardia, a third heart sound, and a pericardial friction rub. The chest radiographs demonstrated cardiomegaly. Transthoracic echocardiography revealed a large pericardial effusion with no evidence of tamponade (Fig. 1). A pericardiocentesis yielded 980 mL of hemorrhagic fluid. Studies of the pericardial fluid revealed a white blood count of 4000/cmm, red blood count of 2,279,000/cmm, 87% segs, 8% lymphs, 5% monos, protein of 4.8 g/dL, glucose of 78 mg/dL, lactate dehydrogenase of 161 U/L, and a positive acid-fast bacillus smear. The patient improved and was discharged home. Cultures of the fluid were negative at the time of discharge. Three weeks later, the patient was readmitted with a clinical presentation consistent with a recurrence of his pericardial effusion. Cultures of the initial fluid were reported at this admission and identified MAI sensitive to amikacin, rifabutin, clofazimine, and clarithromycin. Given these results, clarithromycin, ciprofloxacin, and ethambutol were begun. These antimycobacterial drugs were stopped 1 week later after the patient developed dystonic movements. He was treated with a combination of ritonavir and saquinavir at discharge. However, he continued to be noncompliant with his medication regimen. He died 3 months after his initial pericardiocentesis from complications relating to recurrent pericardial disease.FIGURE 1.: Two-dimensional echocardiography demonstrating a large pericardial effusion (arrow).Discussion. The pericardium is the most common site of cardiovascular involvement in HIV infection [9]. Many specific infective causes of pericardial effusion have been reported [10,11], but documented MAI infection is uncommon and is reported in only a limited number of cases [3–8]. Woods and Goldsmith [3] reported a case of a small pericardial effusion (on echocardiography) in a patient with acquired immunodeficiency syndrome (AIDS) whereby MAI was cultured from the pericardium and fluid. Despite antimycobacterial therapy, this patient died of cardiac dysfunction. Cohen et al. [4] described a patient with a moderately sized pericardial effusion on echocardiography. An emergency pericardiocentesis yielded 300 mL of fluid that was culture positive for MAI. The patient expired on the same day as the pericardiocentesis [4]. Another case of MAI pericardial effusion in patients with AIDS, described by Kerns et al. [5], involved a large pericardial effusion detected by echocardiography. Cultures from the pericardial fluid and pericardium were positive for MAI. With surgical drainage and antimycobacterial drugs, including amikacin, ethambutol, rifampin, and ciprofloxacin, the effusion resolved after 2 months [5]. Choo and McCormack [6] described a symptomatic patient with AIDS with a large pericardial effusion noted by echocardiography. Stool, blood, and pericardial fluid cultures confirmed MAI infection. With removal of 1 L of pericardial fluid and treatment with clarithromycin, clofazimine, rifampin, ciprofloxacin, and amikacin, the patient did not develop recurrence [6]. Turco et al. [7] described a case of culture-proven MAI pericardial effusion (approximately 500 cc drained) whereby the patient probably expired from Staphylococcus aureus sepsis soon after presentation. Most recently, Estok and Frances [8] presented a case involving a female with AIDS and a moderate-sized pericardial effusion. Blood, stool, and pericardial cultures were positive for MAI. Despite antimycobacterial treatment with rifabutin, clofazimine, and ethambutol, the patient expired from disseminated MAI and presumed HIV-associated cardiomyopathy. Conclusions. MAI should be considered as an etiological agent in the differential diagnosis of pericardial effusion in patients with AIDS. The clinical findings of pleuritic chest pain, a pericardial friction rub, and cardiomegaly are commonly encountered. Furthermore, the presence of pericardial effusion predicts a poor prognosis in patients with HIV infection, although the size of the effusion is not prognostic. Finally, MAI pericardial effusions may be effectively treated with antimycobacterial therapy, highly active antiretroviral therapy, and surgical management [1]. However, our case suggests a poor prognosis for patients with a pericardial effusion caused by MAI who do not receive antiretroviral and antimycobacterial therapy.

Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction

OBJECTIVESWe sought to evaluate the prognostic impact of right ventricular (RV) myocardial involvement in patients with inferior myocardial infarction (MI).BACKGROUNDThere is uncertainty regarding the risk of major complications in patients with inferior MI complicated by RV myocardial involvement. Whether these complications are related to RV myocardial involvement itself or simply to the extent of infarction involving the left ventricle (LV) is also unknown.METHODSWe examined the incidence of death and mechanical and electrical complications in patients with (n = 491) and without (n = 638) RV myocardial involvement and in patients with anterior MI (n = 971) in an analysis from the Collaborative Organization for RheothRx Evaluation (CORE) trial. Left ventricular infarct size was assessed by technetium-99m–sestamibi single-photon emission computed tomography and peak creatine kinase, and LV function was assessed by radionuclide angiography. We also performed a meta-analysis in which we pooled the results of our study with previous smaller studies addressing the same question.RESULTSSix-month mortality was 7.8% in inferior MI compared with 13.2% in anterior MI. Among patients with inferior MI, serious arrhythmias were significantly more common in patients with RV myocardial involvement who also had a trend toward higher mortality, pump failure and mechanical complications. However, this was not associated with a difference in LV infarct size or function. A meta-analysis of six studies (n = 1,198) confirmed that RV myocardial involvement was associated with an increased risk of death (odds ratio [OR] 3.2, 95% confidence interval [CI] 2.4 to 4.1), shock (OR 3.2, 95% CI 2.4 to 3.5), ventricular tachycardia or fibrillation (OR 2.7, 95% CI 2.1 to 3.5) and atrioventricular block (OR 3.4, 95% CI 2.7 to 4.2).CONCLUSIONSPatients with inferior MI who also have RV myocardial involvement are at increased risk of death, shock and arrhythmias. This increased risk is related to the presence of RV myocardial involvement itself rather than the extent of LV myocardial damage.

QT dispersion in patients with Takayasu arteritis.

This study was designed to test the hypothesis that myocardial involvement exists in patients with Takayasu arteritis and is associated with increased QT dispersion, which is a marker of repolarization inhomogeneity. Twenty-one consecutive patients with Takayasu arteritis and no significant coronary artery disease were included. Twelve-lead electrocardiogram and exercise-induced thallium-201 myocardial scintigraphy were performed in all patients. Ten of 21 patients (48%) had abnormal findings on scintigraphy. Patients were divided into two groups by the presence (group P, n = 10) or absence (group N, n = 11) of exercise-induced thallium-201 myocardial scintigraphic perfusion abnormalities, including permanent defects in three, reversible defects in four, and slow washout in three. The QT dispersion at rest was significantly greater in group P than that in group N (54 +/- 12 vs 40 +/- 8 msec, p < 0.005). The QTc dispersion at rest was also significantly greater in group P than in group N (59 +/- 15 vs 43 +/- 11 msec, p < 0.01). In patients with Takayasu arteritis, myocardial involvement suggested by exercise-induced thallium-201 myocardial scintigraphic perfusion abnormalities is not rare, even when no significant coronary stenosis is present on angiography. Increased baseline QT dispersion was associated with scintigraphic abnormalities and may be a useful marker of myocardial involvement in patients with Takayasu arteritis.

Visualization of cardiac involvement in patients with systemic sarcoidosis applying contrast-enhanced magnetic resonance imaging.

Contrast-enhanced MRI may serve as a sensitive noninvasive tool for the detection and follow-up of myocardial involvement in patients with systemic sarcoidosis.

A follow up study of myocardial involvement in patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)

ObjectiveTo investigate cardiac function in patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) and clarify the clinical features of cardiomyopathy in MELAS.Patients11 consecutive patients with MELAS (mean age...

M mode and Doppler echocardiographic assessment of left ventricular diastolic function in primary antiphospholipid syndrome.

High titres of serum antiphospholipid antibodies are a possible pathogenic factor for cardiac lesions in patients with systemic lupus erythematosus. To test the hypothesis of a causal link between high titres of antiphospholipid antibodies in the serum and myocardial involvement in patients without systemic lupus erythematosus. 18 patients with primary antiphospholipid syndrome (recurrent fetal loss, arterial and/or venous thrombosis, high titres of antiphospholipid antibodies, and no criteria for systemic lupus erythematosus) were prospectively studied by cross sectional, M mode, and pulsed Doppler echocardiography, and compared with 18 healthy controls. The pulsed Doppler indices of left ventricular diastolic function included isovolumic relaxation time and four mitral outflow indices: peak velocity of early flow, peak velocity of late flow, early to late peak flow velocity ratio, and rate of deceleration of early flow. Four computerised M mode indices were also measured: peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall, and velocity of circumferential chamber lengthening. Compared with controls, patients with primary antiphospholipid syndrome had higher values for isovolumic relaxation time and peak velocity of late mitral outflow and lower values for early to late mitral peak outflow velocity ratio, rate of deceleration of early mitral outflow, peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall and velocity of circumferential chamber lengthening. This abnormal pattern reflects an impairment of myocardial relaxation and filling dynamics of the left ventricle in patients with primary antiphospholipid syndrome who were free of any clinically detectable heart disease. These data suggest that high serum titres of antiphospholipid antibodies may be associated with subclinical myocardial damage.

Intractable heart failure, conduction disturbances and myocardial infarction by massive myocardial invasion of malignant lymphoma

A patient with malignant lymphoma who developed congestive heart failure, conduction disturbances and myocardial infarction is presented. Two-dimensional echocardiography revealed marked thickening of the left ventricular wall, where the gallium scan correspondingly showed an abnormal accumulation. Irradiation to the mediastinum resulted in a dramatic decrease in ventricular wall thickness and disappearance of the gallium accumulation. Postmortem examination confirmed previous lymphomatous involvement of the myocardium. Combined techniques, including echocardiography and gallium scan, can be valuable for noninvasive detection and follow-up of myocardial involvement in patients with malignant lymphoma.

Detection and quantification of acute, isolated myocardial infarction by two dimensional echocardiography

Ninety consecutive patients with acute, isolated myocardial infarction were evaluated with two dimensional echocardiography. Satisfactory echocardiograms were obtained in 66 patients (73 percent). All patients were studied 2 to 12 hours after the onset of symptoms. Sixty patients had additional studies at 48 and 72 hours. Long axis views were obtained at the base, body and apex of the left ventricle. Five short axis views of the left ventricle were obtained at different levels from the cardiac base to the apex. The individual short axis views, corrected for the end-diastolic internal diameter of the left ventricle, were divided into equal segments and the area of asynergy in each view was estimated. Infarct localization was similar on electrocardiography and echocardiography in 62 of 66 patients. In two patients the sites differed. Localization was possible only with two dimensional echocardiography in one patient. The results of an echocardiographic study in one patient were false negative. During the study period the individual asynergic area remained stable. The initial asynergic area correlated well (r = 0.87, p <0.01) with the peak value of the isoenzyme of creatine kinase (CK-MB), which occurred hours later. Thus, two dimensional echocardiography is a reliable method to localize and quantify, early after the onset of symptoms, the eventual extent of myocardial involvement in patients with acute, isolated infarction.

Estimation of myocardial involvement in patients with acute myocardial infarction by two-dimensional echocardiography.

To determine whether real-time two-dimensional echocardiography (2-D echo) can estimate the extent of myocardial involvement in patients with acute myocardial infarction (MI), regional wall motion on serial short-axis 2-D echo recordings was analyzed and the summed scores were compared with estimates of infarct involvement by thallium-201 reperfusion (Tl) and technetium-99m stannous pyrophosphate (99mTc-PYP) scintigraphy. Thirty-two consecutive male patients admitted with their first MI were studied; 10 patients had anterior, 16 had inferior and six had subendocardial MIs. Two patients were technically unsuitable for 2-D echo studies. Twenty patients had Tl scintigrams and 29 had 99MTc-PYP scintigrams. Summed 2-D echo scores correlated closely with estimates of infarct involvement by Tl (r = 0.87) and with estimates of infarct size by 99mTc-PYP (r = 0.74). The location of MI by 2-D echo agreed with the electrocardiographic location in 26 of 29 patients; discrepancies occurred in one inferior and two subendocardial MIs. Predischarge 2-D echo failed to identify extension of transmural infarction. However, two patients whose subendocardial MIs progressed to transmural MIs were identified. This study shows that 2-D echo is a valid method for the early estimation of the extent of myocardial involvement in patients with acute MI, especially transmural MIs. In particular, 2-D echo correlates closely with Tl reperfusion scintigraphy because both detect areas of ischemia and infarction.

Ballistocardiographic study of body acceleration during the acute and convalescent stages of rheumatic fever

Ballistocardiograms of body acceleration, velocity, and displacement were recorded serially in 170 children, ranging in age from 6 to 15 years, during various stages of acute rheumatic fever and during convalescence. Similar records were obtained from a control group of 150 children. Changes in the acceleration ballistocardiogram designated as grossly “abnormal” were encountered in 1.3 per cent of the total control group. There was a direct relationship between the severity of acute rheumatic carditis and the incidence and degree of ballistocardiographic abnormality. The incidence of grossly abnormal ballistocardiograms decreased as the acute rheumatic attack subsided. During treatment with either cortisone or salicylates, the ballistocardiogram appeared to reflect the cardiac status of the patient rather than the symptomatic response to the anti-inflammatory effects of therapy. During the first few months of convalescence, patients with the highest incidence of abnormal ballistocardiograms were those who had had clinically evident carditis during the acute stage of the disease. Within six months, the incidence of gross abnormalities in the BCG's in this group decreased significantly. Patients without apparent carditis during the acute stage of the disease had fewer abnormal BCG's during the first three months of convalescence. All reverted to normal after six months. Progressive improvement in the ballistocardiogram occurred despite the persistence of valvular deformity except in some patients with marked cardiac enlargement. This study indicates that marked acceleration BCG changes occur frequently during the acute stages of rheumatic fever, when rheumatic carditis is clinically evident. When clinical manifestations of carditis are absent such changes appear less frequently and are less marked. During convalescence virtually all abnormalities disappear by the end of six months except in those patients whose cardiac reserve is limited by persistent chronic rheumatic carditis or advanced rheumatic heart disease. The acceleration BCG has many advantages over previously described methods for the measurement of body motion. The absence of quantitative criteria to determine the range of normal variation compels dependence upon subjective impressions which at present impose a serious limitation upon the immediate clinical application of the method. The results of this study, however, justify further investigation of the use of the acceleration BCG to detect myocardial involvement in patients with rheumatic fever.