Current Cardiology Reviews最新文献

Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury has varying definitions, but in general, increased serum creatinine level by ≥ 0.3 mg/dL (26.5 µmol/L) or 1.5x of baseline value or urine output <0.5 mL/kg/h within 1-7 days after contrast media (CM) administration can be considered as CIN. CIN is one of the most common complications and is associated with increased mortality in patients undergoing percutaneous coronary intervention (PCI). Thus, risk stratification for CIN should be made and preventive strategies should be employed in which the intensity of the approach must be tailored to patient's risk profile. In all patients, adequate hydration is required, nephrotoxic medications should be discontinued, and pre-procedural high-intensity statin is recommended. In patients with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, IV hydration should be started 12 hours pre-procedure up until 12-24 hours after the procedure. Remote ischemic preconditioning may be performed pre-procedurally. Radial first approach for vascular access is recommended. During the procedure, low or iso-osmolar CM should be used and its volume should be limited to eGFR x 3.7. In patients at high risk for CIN, additional contrast-sparing strategies may be applied, such as using a contrast reduction system, 5 Fr catheter with no sideholes, CM dilution, limiting test injection, confirming placement using guidewire, use of stent enhancing imaging technology, using metallic/software roadmap to guide PCI, use of IVUS or dextran-based OCT, and coronary aspiration. A more advanced hydration technique based on central venous pressure, left ventricular end-diastolic pressure, or using furosemide-matched hydration, might be considered.

Background: pulmonary arterial hypertension (PAH) is a rare complication of hepatic diseases with portal hypertension that, however, has a significant influence on prognosis. We present a mini-review of how to diagnose and treat it based on a clinical case.

Case presentation: in early childhood, a patient had portal hypertension associated with cavernous transformation of the portal vein. It was successfully treated by reno-splenic surgery. At the age of 20 years, this patient experienced increased dyspnea at minimal physical activity after the hepatic biopsy due to a hepatocellular adenoma. The examination in the specialized unit showed PAH, which was evaluated as associated with portal hypertension (PAH-PoH). The specific two-drug combination therapy was started with prominent improvement in patient's state. Successful surgical tumor treatment was provided some months later. The practical and clinical approaches to the diagnosis and treatment of PAH-PoH are discussed. It was emphasized that not all patients with portal hypertension have pulmonary hypertension, which needs to be treated. A lot of evidence gaps exist in management of these patients.

Conclusion: all patients, even with past history of portal hypertension, should be monitored closely and screened for PAH earlier, for better results of treatment.

Aortic valve insufficiency (AI) describes the pathology of blood leaking through the aortic valve to the left ventricle during diastole and is classified as mild, moderate or severe according to the volume of regurgitating blood. Intervention is required in severe AI when the patient is symptomatic or when the left ventricular function is impaired. Aortic valve replacement has been considered the gold standard for decades for these patients, but several repair techniques have recently emerged that offer exceptional stability and long-term outcomes. The appropriate method of repair is selected based on the mechanism of AI and each patient's anatomic variations. This review aims to describe different pathologies of AI based on its anatomy, along with the different surgical techniques of aortic repair and their reported results.

Heart rate is an important indicator of health and disease and the modulation of heart rate can help to improve cardiovascular outcomes. Besides β-blockers, Ivabradine is a wellestablished heart rate modulating drug that reduces heart rate without any hemodynamic effects. This consensus document was developed with the help of expert opinions from cardiologists across India on effective heart rate management in routine clinical practice and choosing an appropriate Ivabradine-based therapy considering the available scientific data and guideline recommendations. Based on the discussion during the meetings, increased heart rate was recognized as a significant predictor of adverse cardiovascular outcomes among patients with chronic coronary syndromes and heart failure with reduced ejection fraction making heart rate modulation important in these subsets. Ivabradine is indicated in the management of chronic coronary syndromes and heart failure with reduced ejection fraction for patients in whom heart rate targets cannot be achieved despite guideline-directed β-blocker dosing or having contraindication/intolerance to β-blockers. A prolonged release once-daily dosage of Ivabradine can be considered in patients already stabilized on Ivabradine twice-daily. Ivabradine/β-blocker fixed-dose combination can also be considered to reduce pill burden. Two consensus algorithms have been developed for further guidance on the appropriate usage of Ivabradine-based therapies. Ivabradine and β-blockers can provide more pronounced clinical improvement in most chronic coronary syndromes and heart failure with reduced ejection fraction patients with a fixed-dose combination providing an opportunity to improve adherence.

Catheter ablation is an effective and durable treatment option for patients with atrial fibrillation (AF). Ablation outcomes vary widely, with optimal results in patients with paroxysmal AF and diminishing results in patients with persistent or long-standing persistent AF. A number of clinical factors including obesity, hypertension, diabetes, obstructive sleep apnea, and alcohol use contribute to AF recurrence following ablation, likely through modulation of the atrial electroanatomic substrate. In this article, we review the clinical risk factors and the electro-anatomic features that contribute to AF recurrence in patients undergoing ablation for AF.

Tricuspid regurgitation is a cardiac valvular anomaly that consists of the return of blood to the right atrium during systole due to incomplete valve closure. This structure can be visualized on ultrasound between 11 and 14 weeks of gestation in most cases. Despite being a common finding, even in healthy fetuses, the presence of tricuspid regurgitation may be associated with chromosomal and structural abnormalities. The evaluation of tricuspid flow and the presence of regurgitation on first-trimester ultrasound has shown promising results regarding its role in the early detection of aneuploidies, congenital heart defects, and other adverse perinatal outcomes. This review article aims to demonstrate the importance of tricuspid regurgitation as a secondary marker, and consequently, significant benefits of its early detection when added to the combined first-trimester screening. Its value will be discussed, namely its sensitivity and specificity, alone and together with other current markers in the fetal assessment performed in the first-trimester ultrasound.

Heart failure (HF) is a global healthcare burden and a leading cause of morbidity and mortality worldwide. Type 2 diabetes mellitus (T2DM) appears to be one of the major risk factors that significantly worsen HF prognosis and increase the risk of fatal cardiovascular outcomes. Despite a great knowledge of pathophysiological mechanisms involved in HF development and progression, hospitalization rates in patients with HF and concomitant T2DM remain elevated. In this review, we discuss the complex interplay between systemic neurohumoral regulation and local cardiac mechanisms participating in myocardial remodeling and HF development in T2DM with special attention to cardiomyocyte energy metabolism, mitochondrial function and calcium metabolism, cardiomyocyte hypertrophy and death, extracellular matrix remodeling.