Pedro Carrilho-Ferreira

Cystatin C as Prognostic Biomarker in ST-Segment Elevation Acute Myocardial Infarction

Cystatin C is a marker of renal dysfunction, and preliminary studies have suggested it might have a role as a prognostic marker in patients with coronary artery disease. The aim of the present study was to evaluate the usefulness of cystatin C for risk stratification of patients with ST-segment elevation myocardial infarction, regarding in-hospital and long-term outcomes. We included 153 consecutive patients with ST-segment elevation myocardial infarction treated by primary angioplasty. The baseline cystatin C level was measured at coronary angiography. The in-hospital outcome was determined as progression to cardiogenic shock or in-hospital death, and the long-term outcome was assessed, considering the following end points: (1) death and (2) death or reinfarction. Of the 153 patients evaluated (age 61 ± 12 years; 75.6% men), 15 (14.4%) progressed to cardiogenic shock and 4 (2.7%) died during hospitalization. The patients who progressed to cardiogenic shock or died during hospitalization had significantly greater cystatin C levels (1.02 ± 0.44 vs 0.69 ± 0.24 mg/L; p = 0.001). Long-term follow-up was available for 130 patients (583 ± 163 days). Among them, 11 patients died and 7 had reinfarction. A high baseline cystatin C level was associated with an increased risk of death (hazard ratio 8.5; p = 0.009) and death or reinfarction (hazard ratio 3.89; p = 0.021). Furthermore, only high baseline cystatin C levels and left ventricular ejection fraction ≤40% were independent predictors of the long-term risk of death, with synergistic interaction between the 2. In conclusion, cystatin C is a new biomarker with significant added prognostic value for patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention, predicting both short- and long-term outcomes.

Non-compaction Cardiomyopathy: Prevalence, Prognosis, Pathoetiology, Genetics, and Risk of Cardioembolism

Left ventricular non-compaction (LVNC) is thought to arise from arrest of the normal process of trabecular remodeling or “compaction” that takes place during embryonic life and is characterized by the presence of a two-layered ventricular wall, with a compact epicardial layer and a non-compacted endocardial layer. It is an uncommon condition that can occur isolated or in association with other disorders, including congenital heart anomalies and mitochondrial or musculoskeletal disorders. Both familial and sporadic forms are recognized, and several responsible genes have been identified, although only a minority of patients can be successfully genotyped. The diagnosis is usually made by echocardiography, but cardiac magnetic resonance imaging has been used increasingly. Management is mainly empirical and directed at the major clinical manifestations: heart failure, arrhythmias, and systemic embolic events. This article will review the major features of LVNC and present new trends in the diagnosis and management of this intriguing condition.

Circulating miR-122-5p/miR-133b Ratio Is a Specific Early Prognostic Biomarker in Acute Myocardial Infarction

BACKGROUND MicroRNAs (miRNAs) are key players in cardiovascular development and disease. However, not only miRNAs of a cardiac origin have a critical role in heart function. Recent studies have demonstrated that miR-122-5p, a hepatic miRNA, increases in the bloodstream during ischemic cardiogenic shock and it is upregulated in the infarcted myocardium. The aim of the present study was to determine the potential of circulating miR-122-5p as a biomarker for early prognostic stratification of ST-segment elevation acute myocardial infarction (STEMI) patients. METHODSANDRESULTS One hundred and forty-two consecutive STEMI patients treated with primary angioplasty were included in the study. Serum levels of miR-1-3p, -122-5p, -133a-3p, -133b, -208b-3p and -499a-5p were measured at the time of cardiac catheterization by quantitative polymerase chain reaction and related to in-hospital and long-term outcome. During a follow up of 20.8 months, 9 patients died, 6 had recurrence of myocardial infarction, and 26 patients suffered an adverse cardiovascular event. Event-free survival was significantly worse in patients with a higher miR-122-5p/133b ratio (3rd tertile distribution, above 1.42 Log(10)), having almost a 9-fold higher risk of death or myocardial infarction and a 4-fold higher risk of adverse cardiovascular events. CONCLUSIONS This study showed that the miR-122-5p/133b ratio is a new prognostic biomarker for the early identification of STEMI patients at a higher risk of developing major adverse events after undergoing primary percutaneous coronary intervention. (Circ J 2016; 80: 2183-2191).

Carcinoid Heart Disease: Outcome After Balloon Pulmonary Valvuloplasty

Carcinoid heart disease typically presents with pulmonary stenosis and tricuspid regurgitation. Management is intended for symptomatic relief, and valvular intervention is indicated in refractory heart failure. Balloon valvuloplasty is an option for patients not suitable for surgery. We report the case of a patient with a carcinoid tumour, who developed postoperative refractory hypoxemia. Transthoracic echocardiogram revealed carcinoid pulmonary and tricuspid valve disease, with severe pulmonary stenosis. Balloon valvuloplasty was performed with major clinical improvement.

Adult-Onset Still's Disease and Cardiac Tamponade: A Rare Association

Adult-onset Stills disease is a rare disorder with potentially severe clinical features, including cardiac involvement. This systemic inflammatory disease of unknown origin should be considered in the differential diagnosis of pericarditis, with or without pericardial effusion. Cardiac tamponade is a very rare sequela that requires an invasive approach, such as percutaneous or surgical pericardial drainage, in addition to the usual conservative therapy. The authors describe a case of adult-onset Stills disease rendered more difficult by pericarditis and cardiac tamponade, and they briefly review the literature on this entity.

Severe Rheumatic Mitral Stenosis: A 21st Century Medusa

Although the prevalence of rheumatic fever has greatly decreased in developed countries, rheumatic mitral stenosis still causes significant morbidity and mortality. Symptomatic patients have a poor prognosis, with a 0 to 15% 10-year survival rate, particularly if percutaneous or surgical intervention are contraindicated or considered high risk. We present a case of severe rheumatic mitral stenosis with an evolution over 4 decades, in which exceptional venous distention has established.

Eosinophilic myocarditis with left ventricular apical aneurysm.

A previously healthy 27-year-old male patient from Sao Tome and Principe presented with severe oppressive, precordial pain, refractory to medical therapy, and was evacuated to our institution 4 months after presentation. An ECG showed deep, inverted T-waves on inferior and lateral leads. The eosinophil count was elevated (800 cells/μL), without leucocytosis, and the cardiac troponin I was …

Ectasia anulo-aórtica em imagem

A 69-year-old white man was transferred to our hospital with a diagnosis of aneurysm of the ascending aorta and suspected type A acute aortic dissection. The patient had a history of hypertension, irregularly treated, type 2 diabetes and previous smoking (35 pack/years). He had been experiencing progressively worsening fatigue and exertional dyspnea for a year. The present hospitalization was prompted by thoracic and epigastric pain radiating to the back accompanied by dyspnea, with one day of evolution. Physical observation revealed hypertension and a grade IV/VI aortic diastolic murmur. Initial laboratory tests and electrocardiogram were normal. Transthoracic echocardiography showed marked dilatation of the aortic root and ascending aorta (maximum transverse diameter 71 mm) with severe aortic regurgitation. An image suggestive of an intimal flap prompted assessment by transesophageal echocardiography, which confirmed an aneurysmal dilatation of the aortic root and ascending aorta (maximum transverse diameter 71 mm) sparing the aortic arch and the descending aorta. The aortic valve was tricuspid and severe regurgitation was seen, due to malcoaptation of the leaflets. A linear image moving relative to the right coronary sinus, suggestive of an intimal flap, was observed, which could have corresponded to the course