Information has been received from the authors of a published literature article, title as above, concerning a 71 year old female with chronic obstructive pulmonary disease and chronic anaemia and a history of breast cancer who in status post lumpectomy and lymph node dissection 1999. IN Oct 2000, the pt was hospitalized for inferior wall myocardial infraction (OCT 2000) and underwent coronary artery bypass with placement of a saphenous vein graft to the right coronary artery RCA and mitral valve repair. Family history included congestive heart failure, brother at age 59, and myocardial infraction, brother at age 67. In approx Dec 2000 the pt was vaccinated with a dose of Pneumococcal 23v polysaccharide vaccine, manufacturer unknown, and influenza virus vaccine unspecified. Subsequently the pt developed recurrent reversible dilated cardiomyopathy secondary to viral and streptococcal pneumonia vaccine associated myocarditis. Her case was as follows: On 12/29/2000 the pt presented to the Emergency dept after having been awakened by shortness of breath. The pt denied chest pain, palpitations, dizziness, nausea or diaphoresis. She had recently received pneumococcal pneumonia and flu vaccination. Physical examination was significant for an oxygen saturation of 82% on ambient air, lower extremity edema and pulmonary edema on the chest X ray. ECG revealed sinus tachycardia with Q waves noted in the inferior leads and T wave inversions in the same leads. A TTE was performed, which revealed mild left ventricular enlargement, severe segmental LV dysfunction with severe hypokinesis of the septum, anterior wall, apex and distal lateral wall and hypokinesis of the inferior and posterior walls as well, representing a significant interval change from her previous study. The pt was taken to the cardiac catheterization lab where and angiography revealed a paten SVG to the RCA, normal left anterior descending artery LAD, normal left circumflex artery,but now also showed an ejection fraction of 18% with a kinetic inferobasal and mid inferior walls,mild apical hypokinesis, mild anterobasal hypokinesis and severe anterolateral hypokinesis. The pt was managed in the coronary care unit and treated successfully with diuresis, IV inotropic therapy, digoxin, Angiotensin converting enzyme inhibitor and beta adrenergic receptor blockade. The pt was discharged on 1/5/01. In March 2001, the pt was admitted to the hospital for elective bronchoscopy for work up of a recently discovered lung nodule. TTS at this time revealed mild segmental LV dysfunction, severe hypokinesis of the mid and basal inferior and posterior walls. As compared with the study done on the last hospital admission, there was mild improvement in LV function. In late Dec 2001. the pt was readmitted to the hospital with symptoms of upper respiratory tract infection, complaining of shortness of breath, wheezing, and cough production of white sputum. She had recently received her yearly flu vaccination. Her symptoms began 6 days prior to admission. She denied chest pain, nausea, vomiting, diaphoresis, fever, dizziness or palpitations. IV antibiotics and bronchodilators therapy were initiated. On pulmonary examination, crackles were heard and an echocardiogram was performed to assess LV function and valve anatomy. TTE revealed severe global LV dysfunction again worsened from the previous examination. Five days later cardiac catherization was done to evaluate SVG and coronary artery anatomy, revealing 90% stenosis of the proximal segment of the first right posterolateral RCA branch. Ejection fraction at this time was reported to be 39%. There was no evidence of infarction at this time. Repeat TTE, performed as an out pt, on 2/28/02 showed an improvement in LV function with mild segmental LV dysfunction. Over the next 3 years, the pt was followed as an out pt and had routine echocardiograms performed. In Feb and Nov 2002, TTE showed with mild segmental LV dysfunction with akinesis of basal inferior and basal posterior walls and normal function of the repaired mitral valve, In 2002, the pt did not receive the flu vaccine and she did not have any variation if ejection fraction during that year. Ejection fraction remained at approx 54%. In April 2004, the pt presented to the hospital with URI symptoms, complaining of cough, rhinorrhea and shortness of breath starting the night before admission. At this time, the pt also reported orthopnea. It was reported that in Jan 2004 the pt had undergone an exercise thallium test which revealed no ischemia an ejection fraction was 62%. Cardiac biomarkers were elevated. The pt was admitted to the hospital to rule out myocardial infraction and was tested for URI. A TTE revealed severe segmental LV dysfunction with akinesis of posterior and inferior walls and hypokinesis of the remaining segments. Cardiac catheterization was performed an revealed patency of the SVG to the RCA and a patent stent in the first right posterolateral branch of the RCA. There was mild diffuse disease seen in the midsegment of the LAD. During the hospital stay, the pt had non sustained ventricular tachycardia, with was evaluated with electrophysiology and treated medically. The pt was again discharged without complications. Repeat electrocardiogram was performed as an out pt 1 month later, again showing the reversal of LV dysfunction. This TTE revealed mild segmental LV dysfunction. Since then, the pt has done well and continued to follow up on an out pt basis. The authors reported that myocarditis leading to cardiomyopathy was caused by viral upper respiratory infection and post streptococcal pneumonia vaccine. A copy of the published literature article is attached as further documentation of the pts experienced.