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Infections are assumed to play a role in coronary artery disease (CAD) and cardiomyopathies. It is unknown whether the seroprevalence of antibodies to these microorganisms is higher in patients with than without CAD. The seroprevalence of antibodies to Bartonella henselae, Borrelia burgdorferi, Chlamydia pneumoniae, Coxiella burnetii, Helicobacter pylori, human granulocytic Ehrlichia, Leptospira, Rickettsia conorii, and Treponema pallidum was assessed prospectively in patients with exertional dyspnea or anginal chest pain who underwent coronary angiography because of suspected CAD. Patients with normal angiograms (NA) were those in whom no more than 50% stenosis of any coronary artery was found. Patients with CAD were patients who underwent percutaneous transluminal coronary angioplasty. There were 50 patients with CAD (9 female) and 62 with NA (25 female), with a mean age of 62 years. All patients had antibodies to at least one microorganism: to B. henselae, 8% of CAD patients and 5% of NA patients; to B. burgdorferi IgG, 14% CAD and 6% NA; to B. burgdorferi IgM, 6% CAD and 3% NA; to C. pneumoniae lipopolysaccharide (LPS) IgA, 76% CAD and 77% NA; to C. pneumoniae LPS IgG, 80% CAD and 90% NA; to C. burnetii, 0% CAD and 5% NA; to H. pylori, 92% CAD and 68% NA; to human granulocytic Ehrlichia, 8% CAD and 3% NA; to Leptospira IgG, 4% CAD and 2% NA; to R. conorii, 10% in both groups; and to T. pallidum, 2% CAD and 0% NA. The seroprevalence of antibodies to microorganisms known to induce arterial and myocardial damage does not differ between patients with CAD and NA.

In patients with suspected coronary heart disease and normal angiograms, hypertension, neuromuscular disorders, tachycardiomyopathy, hypothyroidism, and hemochromatosis should be considered as possible causes.

We present the case of a 76-year-old female with suspected Friedreich ataxia, in whom leakage and thrombosis of a percutaneously implanted left atrial appendage occluder (PLAATO) was observed 2 years after implantation. Because of late developing leakages and thrombi, regular transesophageal echocardiographic examinations should be carried out in patients with occluded left atrial appendagaes. In view of these complications and the potential important hemodynamic role of the left atrial appendage, the benefit of its occlusion is questionable, and the indications of PLAATO should be strongly reconsidered.The percutaneous left atrial appendage transcatheter occlusion device (PLAATO) is considered a safe and feasible alternative to oral anticoagulation (OAC) in atrial fibrillation (AF) patients with contraindications to OAC. 1 In March 2005, a 74-year-old female with paroxysmal AF, arterial hypertension, and two ischemic strokes with left hemiparesis (in 1989 and 1990), underwent left atrial appendage (LAA) occlusion by a PLAATO system. This procedure had to be performed since the patient did not tolerate OAC, which resulted in hair loss as well as her risk for stroke/embolism being considered as high. LAA occlusion was successful, as documented by transesophageal echocardiography (TEE) and dye injection into the left atrium during the procedure. Postprocedural cranial computed tomography showed no signs of recent ischemia. The patient was released with a therapy of 100 mg aspirin, 75 mg clopidogrel, 20 mg pantoprazole, 4 mg tizanidine, 5 mg bisoprolol, and 10 mg enalapril. After 2 months, TEE showed complete sealing of the LAA without any thrombus on the device. Clopidogrel was discontinued and aspirin 100 mg/day continued.In March 2007, the patient was readmitted because of chest pain. ECG showed AF but no signs of ischemia. Neither blood tests nor perfusion scintigraphy showed signs of myocardial ischemia, why her chest pain was assumed to be musculoskeletal. There were no signs of infection as per the patient's history, clinically, or through laboratory investigations. Chest pain decreased after analgetic drugs and physiotherapy. AF converted spontaneously to sinus rhythm. Clinical neurologic investigation showed postural tremor, intention tremor, dysdiadochokinesia, weakness for hip flexion (M5-) and foot extension (M4-), bilateral foot deformity (Friedreich foot), reduced Achilles tendon reflexes, and atactic stance. Cerebral magnetic resonance imaging (MRI) showed spotted small hyperintense lesions subcortically and in the frontal and parietal, lobes, referring to microangiopathy. Friedreich ataxia and polyneuropathy were suspected.TEE showed a structure measuring 6 × 2 mm in the niche between the LAA wall and the PLAATO device, highly suggestive of a thrombus (Figure 1). Additionally, by color-Doppler, a small jet between the LAA wall and the PLAATO device was detected (Figure 2). Cardiac MRI failed to visualize the jet and the suspected thrombus, due to artifacts deriving from the PLAATO device and the sma...