A simple prognostic model for assessing in-hospital mortality risk in patients with acutely decompensated heart failure.

Background An assessing of the in-hospital mortality risk for an emergency hospitalized patient with acutely decompensated heart failure (ADHF) is challenging task. Simple formula can help. Methods On the base of six indicators identified in derivation group, simple formula for assessing the risk for in-hospital mortality of ADHF patients was derived and later tested in validation group. Results The retrospective analysis of a derivation group (533 survivors, 121 deceased) identified six risk indicators: age, heart rate (HR), systolic blood pressure (SBP) and serum concentrations of urea, sodium (Na) and uric acid (UA). The final formula was created ([age/10]2 × HR/SBP)+(Urea-Na/10)+UA/100 and formula result of 53 was established as cut-off result. In the derivation group, at the cut-off point of 53, area under the ROC curve (AUC) was 0.741 (95% CI 0.701-0.776); with sensitivity 54% and specificity 83%. The discriminative capacity of the formula was significantly higher than each of its components. In the validation group of 591 patients (527 survived, 64 died) AUC was also 0.741 (95% CI 0.706-0.774), sensitivity was 66% and specificity 76%. Positive predictive value (PPV) of the developed formula was modest (34%), but negative predictive value (NPV) was 95%. N-terminal pro-B type natriuretic peptide and troponin I were determined, but not included into formula. Conclusions The developed formula enables simple, rapid and inexpensive risk assessment, but its disadvantage is a low PPV. However, a high NPV permits the identification of patients with a low risk of in-hospital mortality, which could lead to a more rational patient treatment.

Can the difference in serum concentration of urea and cystatin C be used in diagnosis and prognosis of heart failure?

Changes in renal function are an important diagnostic and prognostic indicator in patients with heart failure (HF). They are caused by decreased renal perfusion and consequently decreased glomerular filtration rate (GFR), or by the effect of increased neurohormonal activity (sympathetic nervous system [SNS], rennin-angiotensin-aldosterone system [RAAS] and arginine vasopressin [AVP]). However, the increase of serum concentration of urea, creatinine and other metabolites is not specific for HF. Therefore, it is not possible to distinguish HF from renal diseases solely based on the increase of their concentration, since the increase of their concentration caused by the decrease of GFR cannot be differentiated from the increase due to neurohormonal activity. Urea and cystatin C (Cys C) have different mechanisms of renal elimination, so it can be assumed that in HF their concentrations will not be increased proportionally, what can be used for diagnostic and prognostic purposes. After glomerular filtration Cy C undergoes proximal tubular reabsorption and breakdown, without returning to the blood flow. Since it is not secreted, its serum concentration depends only on GFR. In contrast to Cys C, urea is filtered in glomerulus and subsequently reabsorbed in proximal tubules and collecting duct. Reabsorption of urea is modified by effects of SNS, RAAS and AVP. Therefore its serum concentration depends upon GFR and neurohormonal effect on the tubular function. Since the increase of serum concentration of Cys C is caused only by the effect of the decreased renal perfusion on GFR, while the increase of urea is a result from both decreased GFR and tubular effects of increased neurohormonal activity, the paper hypothesis is that in HF the increase of urea will be significantly higher than the increase of serum Cys C, while in the patients with renal diseases their increase would be mostly proportional. It can be assumed that the disproportion between the increase of Cys C and urea would indicate an increased neurohormonal activity in patients with HF and correlate with its activity. If this hypothesis is proved correct, this parameter could be used in HF diagnosis and risk stratification of such patients.

Primary spontaneous pneumothorax and mitral valve prolapse are not associated.

BACKGROUND: Mitral valve prolapse (MVP) is a common diagnosis in patients with primary spontaneous pneumothorax (PSP). This description assumes that MVP and PSP might be manifestations of a systemic connective tissue abnormality. The purpose of this study was to determine the prevalence of MVP in PSP patients of Croatian origin and evaluate their relationship with connective tissue disorders. We also examined the prevalence of PSP in patients with primary MVP. METHODS: Thirty-two patients with PSP and without underlying pulmonary disease or connective tissue disease underwent two-dimensional transthoracic echocardiography performed by a certified cardiologist. Echocardiography and demographic features were analyzed using descriptive statistics. We also examined the medical records of 60 patients with primary MVP. RESULTS: MVP was found in none of the 32 patients suffering from PSP. The age, sex, smoking status, body mass index, side, rate, and family history were similar to previous investigations. Likewise, none of the 60 patients with primary MVP ever had PSP. CONCLUSION: By applying an updated definition of MVP, we found no MVP case among PSP patients of Croatian origin. We also found no PSP in the primary MVP group. Ethnicity may influence the occurrence of MVP in PSP patients, and PSP in primary MVP patients.

Persistent and progressive ST segment elevation caused by myocardial metastasis.

This is a case of a female patient with collecting duct carcinoma of the right kidney and myocardial metastasis. On electrocardiogram the myocardial metastasis presented with a prolonged and progressive ST elevation and a gradual decrease of the R wave amplitude in leads V3-V6. Echocardiography and autopsy findings confirmed the diagnosis.

Chronic heart perforation with 13.5 cm long Kirschner wire without pericardial tamponade: an unusual sequelae after shoulder fracture.

We report a unique case of cardiac embolization with the Kirschner wire that has been used for osteosynthesis for 24 months previously. According to the complete analysis of medical records and autopsy report, the wire had migrated from the right humeroscapular joint to the heart. Although migration of a Kirschner wire has been reported in the literature, migration of the wire with a total length of 13.5 cm with no pericardial tamponade, despite myocardial perforation, has not been previously described.

The protective effect of mitral stenosis on the embolization of a free-floating left atrial myxoma.

Mitral stenosis associated with free left atrial myxoma is very rare. A free myxoma is life-threatening when incarcerated in the mitral orifice or if embolization of the whole tumor occurs. We report a case of a female patient with moderate mitral stenosis and a detached left atrial myxoma. The myxoma was spherical, solid and smooth-surfaced. Mitral stenosis prevented the exit of the tumor from the left atrium and a possible fatal outcome. The tumor was surgically removed and mitral commissurotomy was successfully performed. Histological analysis confirmed the diagnosis of myxoma.

Pulmonary valve papillary fibroelastoma. A case report.

We present a case of pulmonary valve fibroelastoma diagnosed by echocardiogram which was confirmed by surgical resection in a patient in whom elective coronary artery bypass surgery was performed. The patient had no clinical or constitutional symptoms suggesting the presence of an intracardiac tumor. Routine preoperative transthoracic echocardiography revealed a pulmonary valve tumor. Histopathological analysis resulted in a diagnosis of papillary fibroelastoma. Papillary fibroelastomas are rare and benign cardiac tumors. They usually arise from the cardiac valves. In the literature we found only a few cases, so it seems there is a need for further description of additional cases of pulmonary valve fibroelastoma.

Giant, dissecting, high-pressure pulmonary artery aneurysm: case report of a 1-year natural course.

We report the rare subchronic clinical course of a giant, dissecting pulmonary artery aneurysm in an oligosymptomatic middle-aged woman who had idiopathic pulmonary hypertension. Diagnosis was simple with the use of echocardiography and multislice computed tomography. Conversely, deciding on the treatment was difficult, because prominent surgeons declined to perform surgical repair of the aneurysm and recommended heart-lung transplantation. Therefore, we were forced to treat our patient medically. She survived for 1 year, including 8 months of treatment with sildenafil, and then died suddenly while awaiting transplantation. Our patient, who had a dissecting, high-pressure pulmonary artery aneurysm, had an unexpectedly stable and uneventful clinical course for 1 year, which, under more favorable circumstances, might have provided enough time for heart-lung transplantation to be performed.

Permanent left atrial electromechanical dissociation after conversion of atrial fibrillation in a patient with interatrial block.

In a 52-year-old woman, pharmacological conversion to sinus rhythm was achieved after 31 days of atrial fibrillation. In spite of permanent sinus rhythm, even 7 months after the conversion, no mechanical left atrial activity was restored, although right atrium showed normal contractility.