Takotsubo Cardiomyopathy Presenting with QT Prolongation and Torsade de Pointes in a Patient with Coronavirus Disease 2019.

Coronavirus disease 2019 (COVID-19) is associated with cardiovascular complications; however, Takotsubo cardiomyopathy (TCM) with QT prolongation and Torsade de pointes has been reported only rarely. We present a case of TCM after QT prolongation and Torsade de pointes. A 58-year-old woman was admitted because of COVID-19-related pneumonia. Seven days after admission, she developed sudden loss of consciousness without any indication of cardiovascular disease. A monitoring electrocardiogram indicated Torsade de pointes and a prolonged QT interval. Emergency cardiac catheterization revealed TCM. She was treated with favipiravir and steroids, followed by rehabilitation, and her condition improved. To detect asymptomatic TCM, routine electrocardiography screening should be considered for patients with COVID-19.

Mid-term feasibility and safety of downgrade procedure from defibrillator to pacemaker with cardiac resynchronization therapy.

BACKGROUNDS: Some patients who undergo implantation of cardiac resynchronization therapy with defibrillator (CRT-D) survive long enough, thus requiring CRT-D battery replacement. Defibrillator therapy might become unnecessary in patients who have had significant clinical improvement and recovery of left ventricular ejection fraction (LVEF) after CRT-D implantation. METHODS: Forty-nine patients who needed replacement of a CRT-D battery were considered for exchange of CRT-D for cardiac resynchronization therapy with pacemaker (CRT-P) if they met the following criteria: LVEF >45%; the indication for an implantable cardioverter defibrillator was primary prevention at initial implantation and no appropriate implantable cardioverter defibrillator therapy was documented after initial implantation of the CRT-D. RESULTS: Seven patients (14.2%) were undergone a downgrade from CRT-D to CRT-P without any complications. No ventricular tachyarrhythmic events were observed during a mean follow-up of 39.7 ±â€¯21.1 months and there was no significant change in LVEF between before and 1 year after device replacement (53.5% ±â€¯6.2% vs. 56.4% ±â€¯7.3%, P = 0.197). CONCLUSIONS: This study confirmed mid-term feasibility and safety of downgrade from CRT-D to CRT-P alternative to conventional replacement with CRT-D.

A Fever in Acute Aortic Dissection is Caused by Endogenous Mediators that Influence the Extrinsic Coagulation Pathway and Do Not Elevate Procalcitonin.

Objective A fever is observed in approximately one-third of cases of acute aortic dissection (AAD); however, the causes remain unclear. We investigated the mechanism of a fever in AAD by measuring the serum concentrations of inflammatory markers, mediators of coagulation and fibrinolysis, and procalcitonin, a marker of bacterial infection. Methods We retrospectively studied 43 patients with medically treated AAD without apparent infection. Patients were divided into those with (Group A; n=19) and without (Group B; n=24) a maximum body temperature >38°C. We established which patients fulfilled the criteria for systemic inflammatory response syndrome (SIRS), and its relationship with a fever was examined. Mediators of inflammation, coagulation and fibrinolysis were compared by a univariate analysis. Factors independently associated with a fever were established by a multivariate analysis. Results The criteria for SIRS were fulfilled in a greater proportion of patients in Group A (79%) than in Group B (42%, p=0.001). There was no difference in the procalcitonin concentration between Groups A and B (0.15±0.17 ng/mL vs. 0.11±0.12 ng/mL, respectively; p=0.572). Serum procalcitonin concentrations lay within the normal range in all patients in whom it was measured, which showed that the fever was caused by endogenous mediators. On the multivariate analysis, there was a borderline significant relationship between a fever and the prothrombin time-International Normalized Ratio (p=0.065), likely reflecting the extrinsic pathway activity initiated by tissue factor. Conclusion Our findings suggest that a fever in AAD could be caused by SIRS, provoked by endogenous mediators that influence the extrinsic coagulation pathway without elevating the serum procalcitonin concentration.

Usefulness of rosuvastatin to prevent periprocedural myocardial injury in patients undergoing elective coronary intervention.

The aim of the present study was to investigate whether percutaneous coronary intervention-related periprocedural myocardial infarction (MI) can be suppressed more significantly with high- compared with low-dose rosuvastatin. A total of 232 patients scheduled to undergo elective percutaneous coronary intervention within 5 to 7 days were assigned to groups that would receive either 2.5 or 20 mg/day of rosuvastatin (n = 116 each). The incidence of periprocedural MI did not significantly differ between the high and low-dose groups (8.7% vs 18.7%, p = 0.052). In patients who were not taking statins at the time of enrollment, high-dose rosuvastatin significantly suppressed periprocedural MI compared with the low dose (10.5% vs 30.0%, p = 0.037). The difference was not significant in patients who were already taking statins (high vs low dose 7.6% vs 10.6%, p = 0.582). In conclusion, the incidence of percutaneous coronary intervention-related periprocedural MI was reduced more effectively by high-dose than by low-dose rosuvastatin in statin-naive patients. However, low-dose rosuvastatin is sufficient for patients who are already taking statins.

Therapeutic angiogenesis by controlled-release fibroblast growth factor in a patient with Churg-Strauss syndrome complicated by an intractable ischemic leg ulcer.

Churg-Strauss syndrome (CSS) causes necrotizing vasculitis affecting small- to medium-sized arteries, mainly in the lungs, gastrointestinal system, heart, kidneys, and skin. Skin lesions sometimes ulcerate because of severe ischemia and become intractable when complicated by bacterial infection. We report a rare case of CSS, characterized by a nonhealing ischemic skin ulcer of the right calf with bacterial infection resistant to antibiotics. After sterile maggot debridement therapy, 2 skin autografts failed. Subsequently, a slow-release formula of basic fibroblast growth factor incorporated in biodegradable gelatin hydrogel was administered into the calf muscles to induce vascular regeneration. The ulcer eventually healed with no recurrence. This report describes the use of controlled-release basic fibroblast growth factor for an ischemic leg ulcer in a patient with CSS, suggesting a possible therapeutic role of this novel neovascularization therapy in treating severe skin lesions complicating autoimmune vasculitis syndromes.