Long COVID Complicated by Fatal Cytomegalovirus and Aspergillus Infection of the Lungs: An Autopsy Case Report.

After the acute phase of COVID-19, some patients develop long COVID. This term is used for a variety of conditions with a complex, yet not fully elucidated etiology, likely including the prolonged persistence of the virus in the organism and progression to lung fibrosis. We present a unique autopsy case of a patient with severe COVID-19 with prolonged viral persistence who developed interstitial lung fibrosis complicated by a fatal combination of cytomegalovirus and Aspergillus infection. SARS-CoV-2 virus was detected at autopsy in the lungs more than two months after the acute infection, although tests from the nasopharynx were negative. Immune dysregulation after COVID-19 and the administration of corticoid therapy created favorable conditions for the cytomegalovirus and Aspergillus infection that were uncovered at autopsy. These pathogens may represent a risk for opportunistic infections, complicating not only the acute coronavirus infection but also long COVID, as was documented in the presented case.

Acute limb ischemia due to paradoxical embolism treated with systemic thrombolysis.

We present a case report of a patient with acute upper and lower limb ischemia due to paradoxical embolism. A 67-year old woman without history of venous thromboembolism suffered dislocated patellar fracture requiring surgery in November 2017. Two months after surgery she presented to the emergency room with bilateral pulmonary embolism, occlusion of the left subclavian artery, left common femoral artery and superior mesenteric artery. Transesophageal echocardiography detected patent foramen ovale. Vascular surgeon decided against embolectomy, interventional radiologist against pharmacomechanical thrombolysis due to the extent of the occlusions. Systemic thrombolysis (alteplase) was administered successfully with resolution of the emboli in the left subclavian artery, left common femoral artery and superior mesenteric artery.

[Diuretic treatment in patients with acute pulmonary edema did not produces severe hyponatremia or hypokalemia]. / Diuretická liecba u pacientov s akútnym plúcnym edémom nevyvolala závaznú hyponatriémiu ani hypokaliémiu.

INTRODUCTION: One of the risks of diuretic therapy for pulmonary edema is the development of hyponatremia and hypokalemia with pro-arrhythmic potential. The aim of our study was to analyze the incidence of hyponatremia and hypokalemia after the first day of treatment in a real clinical practice. METHODS: We performed a retrospective analysis of data obtained from medical records. We included all patients with pulmonary edema admitted to the coronary care unit, only patients which died within the first day of treatment were excluded. Absolute dose of administered furosemide, total fluid intake and urine output, saline and pottasium intake were analyzed. Nonparametric paired Wilcoxon test was used to compare natrium and pottasium levels changes. RESULTS: 37 patients were included into analysis. The median dose of furosemide administered during the first day of treatment was 120 mg (IQR 20-300 mg). Median diuresis was 2 400 ml (IQR 1 425-3 225 ml). The median of difference between diuresis and total fluid intake was 315 ml (IQR 538-1 380 ml). Wilcoxon test confirmed a prevailing statistically significant trend of slight rise in serum sodium within the first day of treatment (serum sodium 138.0 IQR 132.8-139.6 vs 138.1 IQR 134,0-141,7 mmol/l, p = 0.0046). The difference in serum potassium was not statistically significant (serum potassium 4.2 IQR 3.9-4.8 vs 4.2, IQR 3.8-4.8 mmol/l). CONCLUSION: Results did not confirmed the need for a substitution of sodium and potassium losses during the first day of diuretic therapy to prevent hyponatriemia and hypokalemia in patients with pulmonary edema.

Right ventricular systolic dysfunction and its prognostic value in heart failure with preserved ejection fraction.

OBJECTIVE: The prognostic impact of right ventricular systolic dysfunction (RVSD) in heart failure (HF) with preserved ejection fraction (HFPEF) is not sufficiently understood. This pilot study evaluates the prevalence and prognostic impact of RVSD in HFPEF. METHODS: Ninety-five consecutive patients, admitted due to HF within one year were included and followed up for 12 months. Patients were classified based on left ventricular ejection fraction (LVEF) into two groups: HFPEF (LVEF >40%; n = 54), and heart failure with reduced ejection fraction (HFREF) (LVEF < or = 40%; n = 41). RVSD was defined as peak systolic tricuspid annular velocity (S') <10.8 cm/s. RESULTS: The prevalence of RVSD was 22% vs 59%, in HFPEF vs HFREF, respectively (P < 0.001). Patients with HFPEF and RVSD had significantly higher one-year all-cause mortality compared to HFPEF with normal RV function (41.7% vs. 4.8%, P = 0.004). The same trend was found in HFREF (33.3% vs. 5.9%, P = 0.057). A similar outcome was obser ved in cardiovascular mortality (H FPEF 33.3% vs. 0%, P = 0.002 and HFREF 20.8% vs. 0%, P= 0.06). RVSD was the only independent predictor of all-cause one-year mortality in patients with HFPEF (HR 11.5, 95% Cl 2.2 to 59.5, p = 0.004). CONCLUSION: RVSD is an independent predictor of all-cause mortality in HFPEF. Patients with HFPEF and RVSD had significantly higher one-year all-cause and cardiovascular mortality than those with normal RV function.

Importance of measurements at or after the J-point for evaluation of ST-segment deviation and resolution during treatment for acute myocardial infarction.

BACKGROUND: Determination of ST-segment deviation (STdev) and its resolution (STR) by reperfusion strategies have become important tools in the assessment of patients with acute myocardial infarction (AMI). STdev has been measured at different time-points, i.e. at 20-80 ms after the J-point. There are no data comparing STR at different time-points. METHODS AND RESULTS: STdev was measured using a new computer-assisted workflow. The intraclass correlation coefficients (ICC) for validity and agreement vs. classical manual measurements (n=1020) were both 0.996 (p<0.0001). The reliability indices were 0.991 (95% CI 0.990-0.992) for the manual vs. 0.995 (95% CI 0.995-0.996) for the computer-assisted method, indicating superiority of the latter. 12-lead STdev were determined on ECGs before (baseline) and 180 min after start of thrombolytic therapy, measured both at the J-point (STdev(J)) and 20 ms after the J-point (STdev(J20); n=2400). STdev(J20) was on average 0.01+/-0.03 mV higher than STdev(J) (p<0.0001) with a tendency towards larger differences for higher ST-elevations (p<0.001). Although the average STR calculated from STdev(J20) and STdev(J) was not statistically different in any infarct location group, in 26% of the patients the difference was >10%, and 11% of the patients were classified into another ST-resolution group. Analysing STdev only in the single lead with the highest ST-elevation at baseline (a simplified measurement which may eliminate the confounding effect of ST-depressions) showed an even higher classification discordance (14% of the patients). CONCLUSIONS: The time-point of STdev measurement is an important variable to be accounted for when evaluating ST resolution data. Uncontrolled extrapolation of classification schemes based on STdev(J20) to other time-points cannot be justified.

ST-deviation reconstruction in missing leads on the 12-lead ECG: applicability in studies on ST-segment resolution during thrombolysis.

Quantitative analysis of ST-segment deviations (STdev) and their resolution by treatment (STR; calculated from a combined sum of STdev in multiple leads) are used in trials on reperfusion for myocardial infarction (MI). Unreadable or unavailable electrocardiogram (ECG) leads are a common reason for exclusion, decreasing the statistical power of the trials. We developed mathematical formulas for reconstruction of immeasurable STdev based on STdev from other available leads on the 12-lead ECG. Formulas were deducted from a database of computer-assisted STdev measurements in 2 ECGs (baseline and 180 min after thrombolysis) of 1121 pts. Their accuracy was later evaluated on a second dataset of 377 pts. Acceptable fits could be derived for absent single leads, or for groups of absent limb leads (I-II-III or aVL-aVF). The intraclass correlation coefficient between real and calculated STdev was >or= 0.80 for each (0.77 for V1 in inferior MI). The correlations between STR calculated from original data and from reconstructed STdev were very strong (all intraclass correlation >or=0.97), and discordance in STR subgroup categorization occurred in