Multiple thromboses, including intracardiac thrombi, accompanied by HIT during ECMO successfully treated with NOACs: A case report.

INTRODUCTION: Unfractionated heparin remains the mainstay of anticoagulation therapy during extracorporeal membrane oxygenation (ECMO) maintenance. However, its continued use in clinical practice exposes patients to the risk of developing heparin-induced thrombocytopenia (HIT). CASE REPORT: A 50-year-old male was diagnosed with multiple thromboses, including an intracardiac thrombi, accompanied by HIT during ECMO after cardiogenic shock related to acute myocardial infarction. The patient was successfully treated with new oral anticoagulants (NOAC), without significant complications. DISCUSSION: HIT during ECMO resulting in multiple thromboses is rare. To our knowledge, this is the first reported case of NOAC use in this context. CONCLUSION: Although thrombocytopenia and thrombosis can occur for various reasons during ECMO maintenance, it is important to consider HIT as a potential cause. NOACs can be considered as a therapeutic option.

Unusual presentation of asymptomatic subacute lead-related ventricular perforation beyond the pericardium without pericardial effusion: a case report.

The clinical manifestations of subacute pacemaker lead-related cardiac perforations are highly variable. Patients with subacute perforations can present with a variety of symptoms, whereas those with acute perforations usually present with cardiac tamponade that necessitates emergent pericardiocentesis. A 32-year-old woman underwent pacemaker implantation for sick sinus syndrome. An active-fixation atrial lead was fixed to the right atrial appendage, and a ventricular lead was fixed to the right ventricle (RV) apex, with acceptable parameters. Two weeks postoperative, the patient visited the clinic for routine examination of the pacemaker parameters. Chest X-ray showed migration of the RV lead beyond the cardiac silhouette. Echocardiography revealed no evidence of pericardial effusion or tamponade. Computed tomography revealed that the RV lead was positioned beyond the RV and pericardium and into the anterior chest wall. Procedural lead revision was performed with cardiothoracic surgery backup. The lead was retracted after loosening the active-fixation screw and inserting the stylet. The lead was placed in the RV septum with active fixation. The procedure was completed without complications, and the patient was discharged after 3 days. Subacute lead perforations can present with various symptoms, and some patients may be asymptomatic without pericardial effusion. Altered lead parameters frequently provide the first indication for the diagnosis of cardiac perforation. Transvenous lead revision with surgical backup is an alternative to surgical extraction.

Correction: Relative bradycardia in patients with COVID-19.

[This corrects the article DOI: 10.1186/s42444-022-00073-z.].

An Unfortunate Combination of Tachycardia and Myocardial Bridge: A Case of Myocardial Infarction Related to Atrial Flutter.

Tachyarrhythmias can lead to chest discomfort, which is usually not severe. However, some patients do complain of severe angina and show evidence of ischemia. As our case study demonstrates, one of the possible mechanisms in these situations is tachyarrhythmia in the presence of an underlying myocardial bridge, resulting in myocardial ischemia due to persistent arterial compression.

ECG features and proarrhythmic potentials of therapeutic hypothermia.

OBJECTIVE: Hypothermia can induce ECG J waves. Recent studies suggest that J waves may be associated with ventricular fibrillation (VF) in patients with structurally normal hearts. However, little is known about the ECG features, clinical significance or arrhythmogenic potentials of therapeutic hypothermia (TH)-induced J waves. METHODS: We analysed ECGs from 240 patients who underwent TH at six major university hospitals in Korea between August 2010 and December 2013. The prevalence, amplitudes and distributions of the J waves and the development of malignant arrhythmia were analysed. RESULTS: The average patient body temperature was 33.5±1.0°C during TH. J waves were observed in 98 patients (40.8%). They were newly developed in 91 cases, and pre-existing J waves were augmented in seven patients. J waves during TH were primarily observed in leads II, III, aVF and V4-6. The average amplitude of the J waves was 0.239±0.152 mV. There were four VF events during TH. These events occurred in three patients who were finally diagnosed with Brugada syndrome, idiopathic VF or early repolarisation syndrome, respectively, and in one patient with non-cardiac aetiology (asphyxia). CONCLUSIONS: J waves were recorded in about 40% of the patients who received TH. They were most frequently observed in the inferior limb leads or lateral precordial leads. Life-threatening VF occurred only rarely (1.7%) during TH and were mainly observed in patients with primary arrhythmic disorder. Although a causal relationship between TH-induced J waves and VF remains unknown, administering TH to this potentially susceptible, high-risk population may require careful attention.

Rosuvastatin Reduces Blood Viscosity in Patients with Acute Coronary Syndrome.

BACKGROUND AND OBJECTIVES: Wall shear stress contributes to atherosclerosis progression and plaque rupture. There are limited studies for statin as a major contributing factor on whole blood viscosity (WBV) in patients with acute coronary syndrome (ACS). This study investigates the effect of statin on WBV in ACS patients. SUBJECTS AND METHODS: We prospectively enrolled 189 consecutive patients (mean age, 61.3±10.9 years; 132 males; ST-segment elevation myocardial infarction, n=52; non-ST-segment elevation myocardial infarction, n=84; unstable angina n=53). Patients were divided into two groups (group I: previous use of statins for at least 3 months, n=51; group II: statin-naïve patients, n=138). Blood viscosities at shear rates of 1 s-1 (diastolic blood viscosity; DBV) and 300 s-1 (systolic blood viscosity; SBV) were measured at baseline and one month after statin treatment. Rosuvastatin was administered to patients after enrollment (mean daily dose, 16.2±4.9 mg). RESULTS: Baseline WBV was significantly higher in group II ([SBV: group I vs group II, 40.8±5.9 mP vs. 44.2±7.4 mP, p=0.003], [DBV: 262.2±67.8 mP vs. 296.9±76.0 mP, p=0.002]). WBV in group II was significantly lower one month after statin treatment ([SBV: 42.0±4.7 mP, p=0.012, DBV: 281.4±52.6 mP, p=0.044]). However, low-density lipoprotein cholesterol level was not associated with WBV in both baseline (SBV: R2=0.074, p=0.326; DBV: R2=0.073, p=0.337) and after one month follow up (SBV: R2=0.104, p=0.265; DBV: R2=0.112, p=0.232). CONCLUSION: Previous statin medication is an important determinant in lowering WBV in patients with ACS. However, one month of rosuvastatin decreased WBV in statin-naïve ACS patients.

Elevated coronary whole blood viscosity in acute coronary syndrome patients.

OBJECTIVES: As most clinical studies measure whole blood viscosity (WBV) from peripheral samples, potential differences in WBV obtained from the coronary arteries are often ignored. This study investigated differences in WBV measured from coronary artery specimens in patients with and without acute coronary syndrome (ACS). METHODS AND RESULTS: Consecutive patients with chest pain who underwent diagnostic coronary angiography were divided into two groups [non-ACS (n = 16), ACS (n = 22)]. The ACS group consisted of unstable angina (n = 13) and acute myocardial infarction (n = 9) patients. Two blood samples were obtained from each patient at the both coronary artery ostia prior to coronary angiography. Low-shear and high-shear blood viscosities (BVs) were measured at shear rates of 1 and 300 s-1, respectively, by a scanning capillary tube viscometer (Bio-Visco Inc., South Korea). Both low-shear and high-shear BVs obtained from peripheral, left and right coronary arteries were not different in both groups. Mean coronary low-shear WBV values obtained in ACS group were 29.2% higher than those in non-ACS group (295.3 ± 87.2 mP vs. 228.5 ± 69.2 mP, p = 0.016). Mean coronary high-shear WBV values obtained in ACS group were 15.6% higher than those in non-ACS group (42.9 ± 10.0 mP vs. 37.1 ± 4.6 mP, p = 0.036). CONCLUSIONS: Direct measurement of WBV from the coronary artery showed no differences with peripheral samples. Future larger studies are needed to clarify our results.

Percutaneous treatment of an injured coronary stent using the looping wire technique.

Drug-eluting stent implantation is an effective treatment for coronary artery disease, yet unexpected serious complications during stent implantation are possible. A 70-year-old man with unstable angina presented with a left main bifurcation lesion. Two drug-eluting stents were successfully deployed at the left main bifurcation lesion by the mini-crush technique under intravascular ultrasound guidance. However, after removal of the wire and intravascular ultrasound catheter, the stent of the proximal left circumflex artery was damaged and shortened at the distal edge. We used a looping wire technique to cross the injured stent and we successfully re-dilated the damaged portion of the stent. Finally, we deployed an additional drug-eluting stent at the left circumflex artery over the damaged stent. Our case illustrates the importance of gentle handling of devices during coronary intervention. Furthermore, interventionists should keep in mind the role of intravascular ultrasound when treating this kind of serious complication.