A 28-year-old patient, medical nurse, in 10th week of her second pregnancy suffered ventricular fibrillation just after entering the waiting room of the emergency department. After she was successfully defibrillated, electrocardiography revealed a large acute anteroseptolateral ST elevation myocardial infarction. Urgent coronarography was done (premedication with 300 mg of aspirin and 600 mg of clopidogrel) with 90 min door-to-balloon time. Proximal left anterior descending occlusion was found, primary percutaneous coronary intervention was done using Amazonia CroCo 3.0/12 bare-metal stent, and Thrombolysis in Myocardial Infarction III flow was achieved. During the procedure, the patient was wrapped in lead apron. Because of postresuscitational agitation, procedure was done in intravenous anesthesia. The revealed risk factors were smoking and hypercholesterolemia. PAI-1 gene 4G/4G genotype and Apo E gene E2/E4 genotype were also found. Estimated X-ray dosage that fetus received during the procedure was 0.45 mSv, which is less than the upper safe limit in pregnancy. All drugs given to our patient (clopidogrel, aspirin, ivabradine, bisoprolol, anesthetics, low-molecular-weight heparin, and unfractionated heparin) have B or C Food and Drug Administration Pregnancy Category. Fetal ultrasonography showed normal fetal growth, and, after consultation with our team, the patient decided to maintain the pregnancy. Before discharge echocardiography showed left ventricle of normal size with anteroseptolateral hypokinesia, small apical aneurysm, left ventricular ejection fraction of 40-45%, and diastolic dysfunction grade II, without pulmonary hypertension. At the 36th week of pregnancy, the patient was hospitalized and closely monitored; clopidogrel and aspirin were discontinued, and low-molecular-weight heparin was administered. She gave birth to a normal boy by vaginal delivery with epidural anesthesia and without any complication.
BackgroundThere are still ambiguities existing in regard to left ventricular non-compaction (LVNC) diagnostic imaging. The aim of our study was to analyze diagnostic potential of late gadolinium enhancement (LGE) and ventricle geometry in patients with LVNC and controls.MethodsData on cardiac magnetic resonance imaging (CMR) studies for LVNC were reassessed from the hospital’s database (3.75 years; n=1975 exams). Matching sample of controls included cases with no structural heart disease, hypertrophic or dilative cardiomyopathy, arrhythmogenic right ventricular dysplasia or subacute myocarditis. Eccentricity of the left ventricle was measured at end diastole in the region with pronounced NC and maximal to minimal ratio (MaxMinEDDR) was calculated.ResultsStudy included 255 patients referred for CMR, 100 (39.2%) with LVNC (prevalence in the studied period 5.01%) and 155 (60.8%) controls. Existing LGE had sensitivity of 52.5% (95%-CI:42.3–62.5), specificity of 80.4% (95%-CI:73.2–86.5) for LVNC, area under curve (AUC) 0.664 (95%-CI:0.603–0.722);p<0.001. MaxMinEDDR>1.10 had sensitivity of 95.0% (95%-CI:88.7–98.4), specificity of 82.6% (95%-CI: 75.7–88.2) for LVNC, AUC 0.917 (95%-CI:0.876–0.948); p<0.001. LGE correlated with Max-Min-EDD-R (Rho=0.130; p=0.038) and there was significant difference in ROC analysis ΔAUC0.244 (95%-CI:0.175–0.314); p<0.001. LGE also correlated negatively with stroke volume and systolic function (both p<0.05, respectively).ConclusionsLGE was found to be frequently expressed in patients with LVNC, but without sufficient power to be used as a discriminative diagnostic parameter. Both LGE and eccentricity of the left ventricle were found to be relatively solid diagnostic landmarks of complex infrastructural and functional changes within the failing heart.
SAŽETAK: Kardiotoksičnost je sve češća nuspojava onkološkog liječenja pa tako i novijih, bioloških ciljanih lijekova. Posebno razvijena monoklonska protutijela ili inhibitori tirozin-kinaze blokiraju bilo receptore HER-2 bilo VEGF bilo pak aktivnost Abl-kinaze. Međutim, time se ometaju i molekularni mehanzimi ključni za kardiovaskularno zdravlje. Anti-HER2 terapija najčešće uzrokuju reverzibilnu sistoličku disfunkciju lijevog ventrikula, a blokadom VEGF receptora razvija se arterijska hipertenzija i povećava sklonost tromboembolijskim incidentima. Ranim prepoznavanjem i liječenjem bolesnika u kojih se razvila kardiotoksičnost postiže se poboljšanje kliničkih ishoda i kvalitete života, a time je često moguće nastaviti specifično liječenja raka. Pri tome su ključni multidisciplinarni pristup kardiologa i onkologa te redovito kardiološko praćenje.SUMMARY: Cardiotoxicity has been increasingly reported as a side effect of oncologic treatment, including novel targeted biological therapy. Specific monoclonal antibodies or tyrosine kinase inhibitors have been developed for blockade of HER2 receptors, VEGF receptors, or Abl kinase activity. However, these actions also interfere with molecular mechanisms that are crucial for cardiovascular health. Anti HER2 therapy generally induces reversible systolic left ventricular dysfunction, whereas VEGF receptor blockade leads to development of arterial hypertension and increased susceptibility to thromboembolic events. In patients developing cardiotoxicity, better clinical outcome and quality of life can be achieved by early recognition and treatment, thus also enabling continuation of anti-cancer therapy in many cases. A multidisciplinary approach including cardiologists and oncologists, along with regular cardiologic follow up, is crucial for successful patient management.KLJUČNE RIJEČI: kardiotoksičnost, kardioonkologija, biološka terapija tumora, inhibitori tirozin-kinaze.
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