IntroductionSarcoidosis is a systemic granulomatous disease which predominantly affects the lungs, although granulomas can also involve all other organs, including the heart. Cardiac sarcoidosis (CS) may occur at any stage of the disease and may be the cause of sudden cardiac death, even in a previously asymptomatic patient. The aim of this study was to evaluate the incidence of CS in a large group of patients diagnosed or followed up due to sarcoidosis.MethodsWe performed a retrospective analysis of patients at our institution discharged with the final diagnosis “sarcoidosis” (ICD-10: D86) from January 2008 to October 2012. Only those with biopsy (from respiratory tract or lymph nodes) confirmed diagnosis of sarcoidosis were included. We then selected the subset of patients with cardiac involvement due to sarcoidosis confirmed by positive magnetic resonance imaging.ResultsThe study covered 1375 consecutive sarcoidosis patients (51 % men), who were hospitalized during 5 years. Multiorgan disease was detected in 160 cases (11.7 %), and cardiac involvement was found in 64 patients (4.7 % of all), 70.3 % of whom were men. Twelve of those with CS were in stage I, 48 in stage II, and four in stage III. The odds ratio for having cardiac involvement in men compared to women was 2.3 (95 % CI 1.36–4.0, p = 0.002).ConclusionsCardiac involvement in sarcoidosis was diagnosed in the similar percentage as in previously published data but was significantly more frequently in men.

Danon disease is a rare X-linked dominant lysosomal glycogen storage disease that can lead to severe ventricular hypertrophy and heart failure. We report a case of Danon disease with cardiac involvement evaluated with cardiovascular magnetic resonance, including late gadolinium enhancement and perfusion studies. Case presentationA 19 year old male with no previous history of heart disease was admitted with rest dyspnoea, found to be due to acute heart failure. He had felt fatigued with progressive limitation of exercise tolerance over the preceding 3 months. Symptoms were exacerbated by an upper respiratory tract infection one month before hospitalization. The patient was treated with antibiotics without noticeable improvement. The patient's mother had died suddenly at the age of 44 with a dilated cardiomyopathy of unknown cause for which she had had a pacemaker implanted.On admission, the patient was cachectic with a body mass index of 17 and in poor general condition, with rest dyspnoea, tachypnoea of 30/minute and tachycardia of 130/ minute. His liver was enlarged, there was evidence of pulmonary oedema and a systolic murmur, maximal at the apex.Blood analysis showed elevated liver enzymes (aspartate aminotransferase 192 units/L; alanine aminotransferase 400 u/L and creatine kinase 510 u/L) and mildly elevated Troponin I and C-reactive protein levels. Chest X-ray confirmed pulmonary oedema and showed an enlarged heart shadow. Sinus tachycardia and left bundle branch block with QRS duration >200 ms were present on electrocardiogram.Echocardiography on admission revealed significantly enlarged left ventricle and both atria, severe hypertrophy of both ventricles muscle without left ventricular outflow tract (LVOT) obstruction. Moderate tricuspid and severe

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The impact of ultramarathon (UM) runs on the organs of competitors, especially elite individuals, is poorly understood. We tested a 36-year-old UM runner before, 1–2 days after, and 10–11 days after winning a 24-h UM as a part of the Polish Championships (258.228 km). During each testing session, we performed an electrocardiogram (ECG), transthoracic echocardiography (TTE), cardiac magnetic resonance imaging (MRI), cardiac 31P magnetic resonance spectroscopy (31P MRS), and blood tests. Initially, increased cholesterol and low-density lipoprotein cholesterol (LDL-C) levels were identified. The day after the UM, increased levels of white blood cells, neutrophils, fibrinogen, alanine aminotransferase, aspartate aminotransferase, creatine kinase, C-reactive protein, and N-terminal type B natriuretic propeptide were observed. Additionally, decreases in hemoglobin, hematocrit, cholesterol, LDL-C, and hyponatremia were observed. On day 10, all measurements returned to normal levels, and cholesterol and LDL-C returned to their baseline abnormal values. ECG, TTE, MRI, and 31P MRS remained within the normal ranges, demonstrating physiological adaptation to exercise. The transient changes in laboratory test results were typical for the extreme efforts of the athlete and most likely reflected transient but massive striated muscle damage, liver cell damage, activation of inflammatory processes, effects on the coagulation system, exercise-associated hyponatremia, and cytoprotective or growth-regulatory effects. These results indicated that many years of intensive endurance training and numerous UMs (including the last 24-h UM) did not have a permanent adverse effect on this world-class UM runner’s body and heart. Transient post-competition anomalies in laboratory test results were typical of those commonly observed after UM efforts.

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