Long term false positive hsTnI on Alinity I probably caused by macrotroponin complex: Case report.

Elevated troponin levels are often indicative of various cardiac diseases; however, analytical interference can lead to false positive troponin concentrations. We present the case of a 48-year-old female patient with persistently falsely elevated high sensitivity troponin I (hsTnI) probably caused by the presence of macrotroponin. Laboratory testing included determination of hsTnI using various analytical methods, serial dilutions and determination of heterophilic antibodies and other autoimmune antibodies. Only precipitation with polyethylene glycol (PEG) indicated the presence of an interference by causing a significant decrease in hsTnI concentration. Our results suggest that the falsely elevated hsTnI concentration could be due to interference with the macrotroponin complex.

NOMOGRAM CONTAINING SIMPLE ROUTINE CLINICAL AND BIOCHEMICAL PARAMETERS CAN PREDICT PATHOLOGIC VENTRICULAR REMODELING IN STEMI PATIENTS.

Heart failure is the leading cause of morbidity and mortality worldwide, with ischemic heart disease being one of the most important etiologic factors. Heart failure develops due to ventricular remodeling, which leads to increases in left ventricular end-systolic and end-diastolic volumes. In this prospective observational study, we included 101 patients with first episode of ST-segment elevation myocardial infarction in whom percutaneous coronary intervention was conducted within 12 h and Thrombolysis in Myocardial Infarction III flow was achieved. The aim was to determine which clinical and biochemical parameters can help predict pathologic ventricular remodeling 1 year after myocardial infarction. We created a nomogram based on routinely used blood tests and vital parameters which showed highest correlation with pathologic ventricular remodeling. The nomogram included NTproBNP value 12 h after reperfusion, aspartate transaminase value 12 h after reperfusion, systolic blood pressure value on admission, and culprit coronary artery. We performed ROC analysis which yielded great predictive value of the nomogram. The area under curve was 0.907 (95% CI 0.842-0.973). The nomogram value of -3.54 had 91.4% sensitivity and 74.0% specificity. We believe that this nomogram, once validated, could offer a widely available, low-cost option that would help identify patients at risk of developing pathologic left ventricular remodeling and achieve this at a very early stage of myocardial infarction (12 h after reperfusion has been achieved).

IDIOPHATIC ASYNCHRONOUS BILATERAL SEGMENTAL TESTICULAR INFARCTION AND ANTICOAGULANT THERAPY: A CASE REPORT.

We present an unusual case of sudden onset of pain in the left testis in a patient with a previous medical history of right orchiectomy due to hemorrhagic infarction. A partial orchiectomy was performed with complete removal of the lesion and reconstruction of the testicular parenchyma. Histopathological assessment confirmed segmental testicular infarction without the presence of malignancy. The patient subsequently received anticoagulant therapy.

Cardiac Amyloidosis Detected on Imaging of Patients with Heart Failure.

BACKGROUND Amyloidosis is a multisystem disease caused by deposition of dysfunctional protein-amyloid-in various organs. The heart is commonly involved, especially in primary (AL) and transthyretin (ATTR) amyloidosis. Most patients present with restrictive cardiomyopathy along with other systemic features of amyloid deposition. Diagnosing amyloidosis is cumbersome and based on the patient's clinical condition and findings from electrocardiography, routine laboratory tests, cardiac biomarkers, imaging, and biopsy. Echocardiography (echo) is a widely available diagnostic imaging method that can help raise suspicion of cardiac amyloidosis (CA) if novel parameters of systolic dysfunction are used, which are based on strain measurement complemented with traditional morphologic and hemodynamic traits. A definitive diagnosis of amyloidosis requires biopsy. It is important to differentiate between AL and ATTR amyloidosis because the treatment approaches for them differ. The prognosis for CA is still dismal but can be improved with early diagnosis and institution of treatment. CASE REPORT Our patients presented with advanced heart failure and subtle clinical signs of amyloidosis. AL amyloidosis was diagnosed based on echo findings and confirmed with bone marrow biopsy. In this report, we describe classic nonspecific echo signs followed by novel parameters of systolic dysfunction. CONCLUSIONS Because the symptoms and signs of amyloidosis are nonspecific, the diagnosis requires a high level of clinical suspicion. Severe diastolic heart failure should prompt a further search for subtle signs on echo that indicate possible amyloid deposition disease. Use of systolic strain analysis increases the specificity of echo for diagnosis of amyloidosis. Echo results combined with specific clinical symptoms and results of a hematology workup can be used to diagnose CA when other, less common tests are not available or invasive testing is not desirable.

Repetitive stent fractures with diffuse coronary artery microaneurysm formation--sirolimus eluting stent hypersensitivity?

While drug eluting stents (DES) are being more widely used in ever more patients receiving DES each day, some new complications may be emerging. Stent fractures and hypersensitivity reactions to stents are among recognized complications that can lead to therapeutic dead end from the interventional cardiologist's point of view. We present a case in which we reached therapeutic dead end with a sirolimus eluting stent, i.e. repetitive stent fractures with diffuse microaneurysms along the implanted DES, possibly due to hypersensitivity reaction to parts of the stent.

Chronic, long-lasting, and untreated gout with concomitant dilated cardiomyopathy and exceptionally vast anasarca: case report.

Gout is the most common type of inflammatory arthritis in man caused by deposition of urate crystals into the joints as the result of elevated serum urate levels. A case of a 59-year-old patient with untreated, long-lasting gout and clinical manifestation of decompensated global dilated cardiomyopathy is presented. Examination revealed generalized pitting edema extending from both lower extremities to the sacrum, abdominal, and thoracic wall, with scrotal swelling and upper extremity involvement, an exceptionally vast generalized edema, i.e. anasarca. Proximal and distal interphalangeal joints of the hands and feet were swollen and deformed, with marked yellow tophi nodules. Laboratory studies revealed high serum uric acid concentration (546 micromol/L), decreased creatinine clearance (0.8 mL/s) and albumin concentration (27.4 g/L), as well as increased total urine protein mass (0.35 g/24 h). X-rays of the affected feet and fists showed punched-out lesions of the subchondral bone with overhanging bony margins in the first metatarsophalangeal, proximal, and distal interphalangeal joints of both hands. The extreme clinical presentation resolved upon intravenous administration of diuretics and pleurocentesis, followed by oral medications including furosemide, angiotensin-converting enzyme inhibitor, spironolactone and digoxin. Since serum urate level has been identified as an independent risk factor for the development of ischemic heart and chronic kidney disease, regulation of urate concentration is necessary, especially in patients diagnosed with gout.