Myocardial involvement associated with infection with Mycoplasma pneumoniae was first reported by Rosner and associates, who described an 18-year-old patient who developed complete atrioventricular block during an upper-respiratory-tract illness. This patient had a change in the complement-fixation test consistent with recent infection with Mycoplasma, but levels of cold agglutinins and serum cardiac enzymes were normal. In a series of 18 patients with asymptomatic myocarditis associated with viral-like illnesses reported by Lewis et al, two patients had serologically proven infection with Mycoplasma. The myocarditis in these two patients was manifested only by abnormalities of the ST-T wave on the ECG and occurred concurrently with respiratory symptoms.
The cold-agglutinin hemolytic anemia associated with infections with Mycoplasma pneumoniae characteristically occurs in the second and third weeks of the illness, with the appearance of cold agglutinins in significant titers (> 1:512). The cold agglutinins are IgM antibodies with anti-I erythrocyte antigen specificity and have a high thermal maximum in those patients who develop hemolytic anemia. El Khatib and Lemer recently reported serologically proven infection with Mycoplasma in a patient with asymptomatic myoperi-carditis and hemolytic anemia associated with a markedly elevated titer of cold agglutinins. Of significant note is the fact that the myocarditis and hemolytic anemia occurred simultaneously on the 22nd day of illness, after resolution of an acute pneumonitis. At no time was the patients anemia severe enough to warrant transfusion.
Our patient initially had severe pneumonia due to Mycoplasma pneumoniae and associated with the syndrome of inappropriate secretion of antidiuretic hormone. The pneumonia appeared to be resolving clinically and radiographically, when the patient experienced sudden clinical deterioration associated with electrocardiographic changes simulating an acute myocardial infarction and a concomitant cold-agglutinin hemolytic anemia. An infarction cannot be entirely ruled out without the benefit of coronary arteriograms; however, the clinical course of increasing dyspnea without associated chest pain, persistent tachycardia, a transient murmur of mitral insufficiency, and extensive electrocardiographic changes which were transient in nature and associated with only minimal cardiac enzymatic elevations are perhaps more consistent with acute myocarditis. The cold-agglutinin hemolytic anemia appeared during the second week of hospitalization, with a markedly elevated titer of cold agglutinins (1:4,096), which had significant activity at 37°C (1:256) and was of characteristic anti-I antibody specificity. The patient experienced no myalgias during her illness.
The association of myocarditis with markedly elevated titers of cold agglutinins and hemolytic anemia suggests an immune basis for this complication. In patients with primary atypical pneumonia, Thomas et al have described cross-reacting antibodies directed primarily against pulmonary tissue, but with occasional reactivity to other tissues, including the heart; however, Kerr and Bridges noted an absence of y-globulin deposits in the cardiac lesions of chicken embryos infected by Mycoplasma synoviae, suggesting a direct toxic effect of the organism.
Although it is difficult to arrive at any definitive conclusions from these data from animals, the clinical presentations suggest that there may be two distinct forms of myocardial involvement associated with infections with Mycoplasma. The first form of myocarditis occurs early in the infection, concomitant with pulmonary parenchymal involvement, and may be related to a direct toxic effect of the infectious agent. The second form, as perhaps demonstrated in our patient, occurs later during the recovery phase and appears to be an immunologically related phenomenon associated with cold hemagglutinin disease.
An alternative explanation for the cardiac involvement in our case should also be considered. Maisel et al presented autopsy evidence of multiple intravascular thromboemboli in a fatal case of infection with Mycoplasma pneumoniae associated with cold hemagglutinin disease. Our patient also had a marked thrombocytosis, which can be associated with an increased incidence of arterial and venous thrombotic complications, particularly in patients with qualitatively normal platelets unassociated with hematopoietic malignant disease.
Thus, it can be speculated that transient embolic occlusion or partial occlusion of the coronary arteries by agglutinated red blood cells or platelets produced the abnormal electrocardiographic and serum enzymatic changes in our patient; however, as noted previously, the rapidity of evolution and the eventual resolution of electrocardiographic changes seem to mitigate this possibility.