Search

While cardiac involvement in the end–stage liver disease (ESLD) is a known condition, the characteristics of cardiac function in cirrhotic cardiomyopathy and their effects on candidates to liver transplant (LT) are still vague. The evaluation of right ventricular failure (RVF) in liver transplant candidates has been revolutionized by advanced cardiac imaging techniques, particularly echocardiography with global longitudinal strain (GLS) analysis. Aim of the present study is to evaluate RV function indexes in ESLD patients candidate to LT and the potential relationship with the liver disease status and cardiovascular major events on early post–LT phase Forty ESDL adult patients (age 46.8 ± 10 yrs, M/F 33/7) candidate to LT (19 for hepatic failure, 18 for hepatocarcinoma and 3 for other causes) were evaluate. All were submitted to transthoracic echocardiography and coronary CT angiography or coronary angiography. The Model for End–stage Liver Disease (MELD) score in the study population was 19±6.8. The higher values of the MELD score (i.e. the worst liver function condition) were directly correlated with the lower RV–GLS (p<0.02). Cardiac function indexes were LV–EF 62.8±4.5%, RV–GLS –22.9±4.5%, LV–GLS –19.5±4.6% and PAPs 31.8±6.6 mmHg. On 21 day follow–up, 4 patients died (2 with acute RV failure, 1 with Tako–Tsubo syndrome). On CT–angiography the value of calcium score was significantly different between the group of fatal events and the rest (0 vs 567±900), revealing that none of the died patient suffered from coronary atheromatic disease. Our findings identified that specific RV–GLS patterns on echocardiography, indicative of subclinical myocardial dysfunction, were strongly correlated with worst clinical hepatic conditions and reduced survival rates post–transplant. The study highlights the importance of advanced cardiac imaging in identifying liver transplant candidates at higher risk of post–transplant mortality due to RHF.

A 75–year–old overweight man, affected by hypertension, diabetes mellitus and atrial fibrillation since 2020. After 3 unsuccessful attempts of electrical cardioversion it was opted for a strategy of rate control with beta blocker and anticoagulant therapy with Rivaroxaban 20 mg. Following episodes of rectal bleeding; adenocarcinoma of the colon was diagnosed. The patient underwent hemicolectomy and started therapy with Pembrolizumab. The anticoagulant was replaced with Edoxaban 60 mg. In August 2022, he was admitted to the emergency department for severe signs and symptoms of heart failure. On ECG, atrial fibrillation with a heart rate of 90 bpm and non–specific changes in ventricular repolarization. The echocardiogram showed a severe reduction of the ejection fraction (FE 30%), which was not present at previous controls. On blood tests, troponins were negative and BNP increased. The patient underwent coronarography which was negative for significant lesions, and heart failure therapy was prescribed. Three months later the patient came to our cardio–oncology outpatient clinic; we repeated the echocardiogram which showed a recovery of the ejection fraction to 45% and planned a cardiac MRI. Cardiac MRI (CMR) showed global left ventricular hypokinesia (FE 42%) and late subepicardial gadoline enhancement in the basal segment of the inferior wall and transmural in the basal segment of the lateral wall without signs of oedema. Report described as compatible with myocarditis. The case was discussed collegially with radiologists and oncologists, and it was decided to discontinue immunotherapy (ICI). Myocarditis is the most common cardiovascular adverse events of ICI therapy, although it has a very low incidence. Generally, myocarditis related to ICI therapy has a high mortality rate and requires discontinuation of ICI. In addition, CMR may have a lower sensitivity in this setting. There is also a possibility of developing left ventricular dysfunction without associated myocarditis in the absence of increase in cardiac troponin and active myocardial inflammation at CMR. Although our case has been defined as myocarditis, it presents some unclear aspects due in part to the early non–diagnosis as a complication of ICI therapy. Although cancer patients taking ICI has expanded considerably in recent years, the evidence on cardiovascular complications is scarce and unknown to the clinical cardiologist.

A 73 year–old man was referred by his general practitioner to our ambulatory for worsening dyspnea. He also reported substantial weight loss (almost 20 kg during the last three months), new onset dysphonia and dry cough. The patient’s medical history also included a former tobacco addiction, arterial hypertension and dyslipidemia. There was not history of cardiomiopathy. Electrocardiogram, showed: sinus rhythm, 60/min with inferior and anterior–lateral abnormality of repolarization. No laboratory exams were available at the first visit. An echocardiogram was performed, showing: marked septal hypertrophy (IVSd= 23 mm), septal hypokinesia, with an ejection fraction at lower limits of normality (EF= 54%), neither systolic anterior motion of the mitral valve. Minimal pericardial effusion was seen. We required a CT scan of the chest, that showed a large (5x8x11cm) mass in the left upper lobe with ipsilateral mediastinal lymphadenopathy. The mass directly extended into the mediastinum with infiltration of pericardial leaflet, left atrium and the left wall of the aortic arch. A hypodense formation of approximately 4 cm in the interventricular septum in the apical portion was reported. PET–CT with FDG was performed, which documented hypercaptation of the radioactive tracer at the level of the above–mentioned lesions. The patient underwent fine–needle aspiration biopsy of the lung mass and the histological examination led to the diagnosis of squamous cell carcinoma of the lung. Systemic treatment with carboplatin plus placlitaxel and pembrolizumab was subsequently started. A cardiac CMR was performed, which documented an area of 30x17x31 mm located at the septal (mid–apical portion), apex and parapical portion of the free wall of the right ventricle with transmural extension. At this area, extensive late gadolinium enanchement (LGE) at marginal level with a central non–capillary core and hyperintense in T2 sequences (compatible with central necrotic lesion). The pericardium also showed LGE and a mild pericardial effusion (maximum 8 mm); left atrium involvement, seen on CT, was not documented . After he completed the third cycle of CHT, at 5 months from the diagnosis, the echocardiogram showed a substantial disappearance of the mass infiltrating the interventricular septum without evidence of pericardial effusion. The ecg was substantially unchanged. The patient stopped carboplatin and paclitaxel after 3 cycles and kept maintenance pembrolizumab still ongoing.

39–year–old female, without cardiovascular risk factors. At the end of pregnancy she complained of progressive dyspnoea and so she was admitted to the emergency room. Blood tests showed elevated D–dimer and LDH values. A chest CT scan was performed showing a mediastinal mass of about 15 cm encompassing the ascending aorta, the left brachiocephalic trunk and the superior vena cava, both of which appeared thrombosed. Therapy with low molecular weight heparin was started. The patient underwent a mediastinal biopsy, which documented a primary mediastinal non–Hodgkin‘s lymphoma. The baseline cardiological evaluation showed a preserved ejection fraction (60%) at echocardiogram (ECHO). The first cycle of chemotherapy with R–CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine) was started. After an episode of hypoesthesia of the left upper limb, that regressed spontaneously within a few hours, she performed MRI that showed multiple areolas compatible with ischemic disease. Following these results the patient was submitted to an ECHO with saline solution injected through the right brachial vein that documented evidence of early opacification of the left atrium and subsequent opacification of the right sections (after 3 cardiac cycles) (Fig. 1–2). This finding suggested a right–to–left shunting, via the bronchial lower district to the left atrium (pulmonary veins). This suspicion was confirmed by CT angiography, which showed occlusion of the superior vena cava with passage of contrast into azygos and early opacification of peribronchial venous circles (Fig. 3). A patency of foramen ovale was ruled out by injection of saline solution through the femoral vein. After the second cycle of chemotherapy, ECHO showed diffuse hypokinesia and reduced EF to 50%. It was then decided to proceed with the third cycle according to the intensified R–DAEPOCH scheme, except for doxorubicin, because of the cardiotoxicity developed by the patient. A cardioprotective therapy was also started with bisoprolol and ramipril with rapid titration. At subsequent radiological controls, a progressive reduction of the mediastinal mass was found and after just one month, the echocardiogram showed a complete recovery of the EF. Contrast injection confirmed presence of a veno–venous shunt. Cardio–oncology is an intriguing and complex discipline that requires the development of local multidisciplinary teams for challenging situations that patients with cancer may ask us to address.

A 53–year–old woman was admitted for chest pain for over two weeks, fever, dry cough, fatigue and myalgia. Chest pain increased in supine position and inspiration. Nasopharyngeal swab was positive for SARS–CoV–2 RT–PCR assay. Admission ECG displayed mild ST–segment elevation (0,5 mm) in inferolateral leads and echocardiogram showed normal left ventricular volume, mildly decreased left ventricular EF (52%) and no regional wall motion abnormalities. Blood tests exhibited elevated values of high–sensitivity troponin I (818 pg/mL), proBNP (19.190 pg/mL), CRP (42 mg/dL), D–Dimer test (1090 ng/mL) and WBC (13000/uL, N 89%, L 7%). IL–6 resulted slightly increased (18 ng/mL). ECG after 24 hours showed T wave inversion in inferolateral leads. Coronary CT angiography revealed normal epicardial arteries. A new echocardiogram, after five days, showed infero–basal hypokinesia, improved global EF (57%) and minimal pericardial effusion. Aspirin and fondaparinoux were started. Myopericarditis was suspected and high dose steroids were administered. After a few days, symptoms improved and ECG, echocardiographic abnormalities and troponin levels were normalized. At 6 weeks follow–up the patient was asymptomatic, ECG and echocardiogram were both normal. Instead cardiac MRI showed signs of endothelial injury: presence of interstitial oedema in the inferoapical and anteroseptal wall (STIR–T2–weighted), without late gadolinium enhancement. We measured blood levels of endothelial dysfunction markers: soluble ICAM–1, VCAM–1 and von Willebrand factor (vWF). They all resulted elevated as compared to a laboratory pool of normal serum (535 ng/ml, 265 ng/ml, and 1659 ng/ml, respectively). Our case was suggestive of myopericarditis related to Sars–Cov–2, but echocardiogram and MRI did not show signs of myocarditis permanent damage. However MRI showed interstitial oedema and hyperemia, typical signs of endothelial injury. Moreover we found high levels of soluble endothelial adhesion molecules, vWF, ICAM–1 and VCAM–1, likely expression of the microcirculatory endothelial dysfunction due to myocardial endothelialitis.In conclusion, our case report suggests that, in COVID–19, acute myocardial injury associated with clinical and investigational signs of myocarditis can be due to myocardial endothelialitis rather than true myocarditis and that an early management with anti–inflammatory drugs (steroids) can be particularly beneficial in patients with unexplained elevated cardiac troponin.

We undertook this study to determine the use of transthoracic and transesophageal echocardiography in detecting valvular perforation and the clinical impact of the latter on the outcome of left-sided infective endocarditis. Transthoracic echocardiography was performed in 58 consecutive patients with infective endocarditis. According to the study protocol, a subgroup of 42 patients also underwent transesophageal echocardiography. At referral, 20 (34%) of 58 patients had echocardiographic evidence of valvular perforation (group A). No valvular perforations were found in the remaining 38 patients (group B). During a follow-up period of 27 +/- 16 months, a major complication occurred in 18 of 20 patients in group A and in 11 of 38 patients in group B (p < 0.0001). Univariate analysis indicated previous infective endocarditis, aortic involvement, and New York Heart Association functional class had a predictive value for valvular perforation (p < 0.001). Stepwise regression analysis confirmed aortic valve perforation as the only independent predictive variable for surgery and death. Valvular perforation is a common complication of infective endocarditis and is associated with an adverse outcome. Transthoracic echocardiography can detect or suggest valvular perforation in infective endocarditis, but transesophageal echocardiography better defines this complication and predicts severe heart failure or the need for early surgical management. (Am Heart J 1997;134:656-64.)

Paradoxical embolism is considered a relatively uncommon disease. Continuous biplane transesophageal echocardiography (TEE) was performed in a 64-year-old woman who had an acute pulmonary embolism. TEE showed an elongated formation highly mobile within both atria. It was trapped in the interatrial septum, passing through a patent foramen ovale. Systemic embolism of the right arm was noted. The patient died 5 hours after admission, and postmortem examination confirmed the diagnosis of pulmonary embolism. This case demonstrates the potential utility of TEE in the study of patients with suspected paradoxical embolism.