Treatment With EkoSonic™ Endovascular System (EKOS®) of Massive Pulmonary Thrombosis Following Recovery From COVID-19 Infection.

COVID-19 infection caused by the new coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an infection with symptoms and results ranging from mild flu-like symptoms to severe respiratory failure leading to death. The risk of thrombosis increases due to hypercoagulation in COVID-19 infection. All causes (endothelial injury, stasis, and hypercoagulopathy) known as Virchow's triad contribute to thrombosis in COVID-19 infection. However, the pathogenesis of hypercoagulability in COVID-19 is still unknown. In this article, we discuss the unique multiple thrombosis events following recovery from COVID-19 infection and our treatment strategy for pulmonary thrombosis. The patient had symptoms of dry cough, fever, and myalgia two months ago. His polymerase chain reaction (PCR) test for COVID-19 was positive, but there was no need for hospitalization. His symptoms resolved within seven days. But, thrombosis of the superior mesenteric artery (SMA) occurred one month after the COVID-19 infection, and bowel resection was performed. He was admitted to our hospital with dyspnea, chest pain, palpitations, and hoarseness. Further evaluation showed tachycardia, hypotension, tachypnea, and anxiety. Peripheral oxygen saturation (SpO2) was 86% at room air. He had hemodynamic instability, right ventricular (RV) dysfunction, and D-Dimer elevation. Pulmonary Embolism Severity Index (PESI) was calculated as 149. The patient was in the high-risk group. Our Pulmonary Embolism Response Team (PERT) decided to apply catheter-directed thrombolysis (CDT) for the treatment of pulmonary thrombosis. The EkoSonic™ Endovascular System (EKOS) (Boston Scientific Corporation, Marlborough, USA) was used for the treatment.

Does aspirin use prevent acute coronary syndrome in patients with pneumonia: multicenter prospective randomized trial.

OBJECTIVES: The aim of this study was to test the hypothesis that aspirin would reduce the risk for acute coronary syndromes (ACSs) in patients with pneumonia. BACKGROUNDS: Pooled data suggest that pneumonia may trigger an ACS as a result of inflammatory reactions and the prothrombotic changes in patients with pneumonia. Hypothetically considering its antiaggregating and anti-inflammatory effects, aspirin might also be beneficial for the primary prevention of ACS in patients with pneumonia. METHODS: One hundred and eighty-five patients with pneumonia who had more than one risk factor for cardiovascular disease were randomized to an aspirin group (n=91) or a control group (n=94). The patients in the aspirin group received 300 mg of aspirin daily for 1 month. ECGs were recorded on admission and 48 h and 30 days after admission to assess silent ischemia. The level of high-sensitivity cardiac troponin T was measured on admission and 48 h after admission. The primary endpoint was the development of ACS within 1 month. The secondary endpoints included cardiovascular death and death from any cause within 1 month. RESULTS: The χ-test showed that the rates of ACS at 1 month were 1.1% (n=1) in the aspirin group and 10.6% (n=10) in the control group (relative risk, 0.103; 95% confidence interval 0.005-0.746; P=0.015). Aspirin therapy was associated with a 9% absolute reduction in the risk for ACS. There was no significant decrease in the risk of death from any cause (P=0.151), but the aspirin group had a decreased risk of cardiovascular death (risk reduction: 0.04, P=0.044). CONCLUSION: This randomized open-label study shows that acetyl salicylic acid is beneficial in the reduction of ACS and cardiovascular mortality among patients with pneumonia.

Interatrial block and P-terminal force: a reflection of mitral stenosis severity on electrocardiography.

BACKGROUND AND AIM OF THE STUDY: Interatrial block (IAB), a frequently overlooked conduction delay between the atria, is defined as prolonged P-wave on the electrocardiogram (ECG). Previously, IAB has been shown to be an indicator of dilated and impaired left atrial function, and a predictor of both atrial fibrillation and embolic stroke. The study aim was to test the hypothesis that, on ECG, IAB with P-terminal force can reflect the echocardiographic severity of mitral stenosis (MS). METHODS: Patients with rheumatic MS who were referred to a single cardiac center for echocardiography between July and October 2009, and who met the study entry criteria (echocardiographically documented rheumatic MS), were invited to participate. Consequently, 116 such patients were studied prospectively, while a group of age- and gender-matched subjects without echocardiographic signs of rheumatic valve involvement served as controls. Transthoracic echocardiography was performed in all subjects. RESULTS: A positive correlation was observed between IAB (> or = 120 ms) and the mean mitral valve gradient (R = 0.3, p <0.001). A strong negative correlation was also present between the mitral valve area (MVA) and the presence of IAB (R = -0.3, p <0.001). The presence of pulmonary hypertension and a poor NYHA functional class were associated with a high incidence of significant IAB (R = 0.4, p <0.001; R = 0.3, p <0.001, respectively), and there was a strong correlation between IAB and the P-terminal force (p <0.001). Both, the presence of significant IAB and P-terminal force were correlated with a calcific mitral valve (p <0.001). Only the MVA (beta = 0.3; p = 0.008) was a predictor of IAB in multivariate analysis. CONCLUSION: A severe mitral gradient, a decreased MVA, an increased pulmonary artery pressure, and a poor NYHA class were shown to correlate with IAB duration and P-terminal force. Significant IAB (> or = 120 ms) and P-terminal force might be considered as a novel indicator of echocardiographic severity and associated complications during the follow up of MS. However, these interrelations must be clarified in further studies.

Fragmented QRS is predictive of myocardial dysfunction, pulmonary hypertension and severity in mitral stenosis.

Reliable non-invasive new indices reflecting severity of rheumatic valve disease would be highly beneficial. Recently, presence of fragmented QRS (fQRS) in ECG was accepted as a marker of myocardial fibrosis. fQRS is defined as the presence of RSR' patterns such as additional R wave (R'), notching in the R wave or the S wave in 2 contiguous leads. Purpose of our study was to establish frequency of fQRS in isolated rheumatic mitral stenosis compared with control group. We studied 193 patients with mitral stenosis and age/gender matched 97 healthy subjects. Patients were categorized according to the New York Heart Association (NYHA) functional class. Severity of mitral stenosis, left ventricular ejection fraction, and pulmonary artery pressure were obtained by means of echocardiography. fQRS was defined on routine 12-lead ECG. fQRS was more frequent in subjects with mitral stenosis than in control group (p < 0.001). fQRS was associated with low ejection fraction, pulmonary hypertension, poor functional NYHA class, increased mean mitral valve gradient and decreased mitral valve area (R = 0.1, p = 0.02; R = 0.1, p = 0.001; R = 0.1, p = 0.01; R = 0.1, p = 0.04; and R = -0.1, p = 0.009, respectively). Mitral valve area was the only independent predictor of fQRS in multiple logistic regression analysis. In conclusion, fQRS is predictive of severe mitral stenosis, lower ejection fraction, increased pulmonary artery pressure, and poor functional class. fQRS might be considered as a novel indicator of mitral stenosis severity and associated complications.

Coronary sinus dilatation is associated with left ventricular systolic dysfunction and poor functional status in subjects with chronic heart failure.

BACKGROUND AND AIMS: Reliable echocardiographic markers additional to plasma biomarkers that would establish prognosis of chronic heart failure and guide therapeutic approach would be beneficial. In our hypothesis, echocardiographic assessment of coronary sinus anatomic alteration, which has been ignored, may be part of remodeling process in heart failure. We also aimed to evaluate relationship between coronary sinus anatomic alteration and left ventricular systolic dysfunction. We echocardiographically analysed 112 patients with heart failure and 61 normal subjects. Left/right ventricular volumes, left atrial area and mean coronary sinus were measured. Coronary sinus diameter was significantly higher in patients than in control group. Statistically positive correlation were present between coronary sinus measurements and left/right ventricular volumes (R = 0.5, P < 0.001; R = 0.4, P < 001, respectively), left atrial area (R = 0.6, P < 0.001), NYHA class (R = 0.3, P < 0.001), mitral regurgitation (R = 0.329, P < 0.001), tricuspid regurgitation (R = 0.215, P < 0.02) and left ventricular mass (R = 0.482, P < 0.001). Statistically negative correlation were present between coronary sinus measurements and left ventricle ejection fraction (R = -0.4, P < 0.001). However, coronary sinus diameter was not correlated with body surface area and pulmonary artery pressure. Tricuspid and mitral regurgitation, left ventricular mass, ejection fraction and functional class were included in multivariate analysis and only ejection fraction was independent predictor of coronary sinus diameter (P = 0.012). We demonstrated that, dilated coronary sinus is possibly a part of entire process of cardiac remodeling and echocardiographic assessment of dilated coronary sinus may provide useful additional information, predicting the severity of chronic heart failure and poor functional class.

Cryptogenic stroke in two cases with left atrial band: coincidence or cause?

Congenital left atrial band (LAB) has been reported previously. However, clinical significance of the LAB has not been clearly defined. Although LAB is generally known as a benign entity, it has been reported to be associated with Chiari's network, patent foramen ovale, mitral valve prolapse, mitral regurgitation, and supraventricular arrhythmias. In this case report we report LAB in a 34-year-old male and 56-year-old female with cryptogenic stroke. To our knowledge, the association of LAB with cardioembolic events has not been reported previously. Lack of other potential risk factors of cardioembolic stroke and normal laboratory examinations lead us to suggest that LAB might be the cause of cardioembolism in the present two cases. In conclusion, in cases with ischaemic stroke, especially the ones with undetermined aetiology, LAB should be kept in mind as a potential cause of cardioembolism.