Continuous cardiac output measured with a Swan-Ganz catheter reacts too slowly in animal experiments with sudden circulatory failure.

BACKGROUND: In many animal experiments, it is vital to detect sudden changes in cardiac output (CO). This porcine study compared CO that was measured with a Swan-Ganz pulmonary catheter with the gold standard (which was a transit-time flow probe around the pulmonary artery) during interventions that caused hemodynamic instability. METHODS: In one series, 7 pigs were exposed to sudden changes in CO. In another series, 9 pigs experienced more prolonged changes in CO. All the pigs had a Swan-Ganz catheter placed into the pulmonary artery and a flow probe around the pulmonary artery. Adrenaline infusion and controlled hemorrhage were used to increase and decrease CO, respectively. The measurements of CO before and after each intervention were compared for correlation, agreement, and the time delay that it took each method to detect at least a 30% change in CO. A Bland-Altman test was used to identify correlations and agreements between the methods. RESULTS: In the first series, there was a delay of 5-7 min for the Swan Ganz catheter to register a 30% change in cardiac output, compared with the flow probe. However, during prolonged changes in CO in the second series, there was a good correlation between the 2 methods. Mixed venous oxygen saturation reacted faster to changes than did CO; both were measured via the Swan-Ganz catheter. CONCLUSIONS: In many animal studies, the use of Swan-Ganz catheters is suitable; however, in experiments with sudden hemodynamic instability, the flow probe is the most advantageous method for measuring CO.

Granulomatosis with polyangiitis and cardio vascular co-morbidity in Denmark. A registry-based study of 21 years of follow-up.

OBJECTIVES: To describe the epidemiology of granulomatosis with polyangiitis (GPA) in Denmark. To investigate if cardiovascular (CV) related comorbidity and death were increased among Danish AAV patients registered with a diagnosis of granulomatosis with polyangiitis (GPA) in Denmark. To investigate if there was a temporal relation between diagnosis of GPA and CV disease and death. METHODS: A population-based cohort study was performed using the Danish Civil Registration System, the Danish National Patient Registry and the Danish Cause of Death Register in the period January 1, 1995, to December 31, 2015. Patients registered twice or more with a diagnosis of GPA were included. Annual incidence rate (IR), point prevalence (PP) and standardized mortality rate (SMR) were calculated. The entire adult population in Denmark served as control population. CV morbidity and death caused by CV disease was registered. RESULTS: We identified 1829 individuals with GPA. The median annual IR was 20.5/1,000,000 and PP increased from 64 to 277/1,000,000 in 2015. Overall SMR was 2.14. Among patients with GPA 171 had a hospital diagnosis of acute myocardial infarction (AMI). Compared to the control population, the hazard ratio (HR) of AMI was 2.47 (95% CI 1.24-4.94) during the first 3 months after the GPA diagnosis. From 3 months to one year declining to 1.41 (95%CI 0.80-2.49) and after 10 years the HR was still slightly increased to 1.64 (95%CI 1.20-2.23). The risk of a diagnosis of heart failure (HF) was markedly increased with a HR at 7.22 (95% CI 4.55-11.46) during the first 3 months after a GPA diagnosis, after three months up to one year 2.94 (95%CI 1.87-4.69), and 2.07 (95% CI 1.54-2.78) after 10 years. The total number of CV deaths in the GPA cohort was 307. During the first three months after a GPA diagnosis, the HR was increased to 9.51 (95%CI 7.12-12.70) declining to 2.51 (95% CI 1.77-3.58) after one year, but still increased to 1.56 (95% CI 1.23-1.98) after 10 years. Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation. CONCLUSION: In a population-based study on GPA, we found stable incidence, increasing prevalence and an overall increased SMR. The risk of CV comorbidity and of CV death among patients with a register diagnosis of GPA was increased.

Risk of Developing Hypokalemia in Patients With Hypertension Treated With Combination Antihypertensive Therapy.

Little is known about the occurrence of hypokalemia due to combination therapy for hypertension. Using data from Danish administrative registries, we investigated the association between different combinations of antihypertensive therapy and risk of developing hypokalemia. Using incidence density matching, 2 patients without hypokalemia were matched to a patient with hypokalemia (K, <3.5 mmol/L) on age, sex, renal function, and time between index date and date of potassium measurement. Combination therapies were subdivided into 10 groups including ß-blockers (BB)+thiazides (BB+thiazides), calcium channel blockers (CCB)+renin angiotensin system inhibitors (RASi)+thiazides (CCB+RASi+Thiazides), calcium channel blockers+thiazides (CCB+thiazides), and ß-blockers+renin angiotensin system inhibitors+thiazides (BB+RASi+thiazides). We used conditional logistic regression to estimate the odds of developing hypokalemia for different combinations of antihypertensive drugs within 90 days of combination therapy initiation. We matched 463 patients with hypokalemia to 926 patients with normal potassium concentrations. The multivariable analysis showed 5.82× increased odds of developing hypokalemia if administered CCB+thiazides (95% CI, 3.06-11.08) compared with CCB+RASi. Other combinations significantly associated with increased hypokalemia odds were BB+thiazides (odds ratio, 3.34 [95% CI, 1.67-6.66]), CCB+RASi+thiazides (odds ratio, 3.07 [95% CI, 1.72-5.46]), and BB+RASi+thiazides (odds ratio, 2.78 [95% CI, 1.41-5.47]). Combinations of thiazides with CCB, RASi, or BB were strongly associated with increased hypokalemia risk within 90 days of treatment initiation.

Association between serum potassium levels and short-term mortality in patients with atrial fibrillation or flutter co-treated with diuretics and rate- or rhythm-controlling drugs.

AIMS: We investigated the association between potassium levels and 90-day all-cause mortality in atrial fibrillation or flutter (AF) patients co-treated with diuretics and rate- or rhythm-controlling drugs. METHODS AND RESULTS: During 2000-12, first-time AF patients treated with beta-blockers, amiodarone, sotalol, verapamil, or digoxin combined with any diuretic within 90 days post-AF discharge were included. Following co-treatment, a potassium measurement within 90 days after initiating diuretic treatment was required. Mortality risk associated with potassium <3.5, 3.5-3.7, 3.8-4.0, 4.5-4.7, 4.8-5.0, and >5.0 mmol/L (reference: 4.1-4.4 mmol/L) was assessed using multivariable Cox regression. In total, 14 425 AF patients were included (median age: 78 years; women: 52%). Patients most often received beta-blocker monotherapy (29%), beta-blockers and digoxin combined (25%), digoxin monotherapy (24%), amiodarone monotherapy (3%), and verapamil monotherapy (3%). Increased 90-day mortality risk was associated with <3.5 mmol/L [hazard ratio (HR) 2.05, 95% confidence interval (CI) 1.68-2.50], 3.5-3.7 mmol/L (HR 1.28, 95% CI 1.05-1.57), 4.5-4.7 mmol/L (HR 1.20, 95% CI 1.02-1.41), 4.8-5.0 mmol/L (HR 1.37, 95% CI 1.14-1.66), and >5.0 mmol/L: (HR 1.84, 95% CI 1.53-2.21). Compared with beta-blocker monotherapy, rate- or rhythm-controlling drugs did not modify the association between potassium groups and mortality risk. CONCLUSION: In addition to hypo- and hyperkalaemia, low and high normal range potassium levels were associated with increased 90-day mortality risk in AF patients co-treated with diuretics and rate- or rhythm-controlling drugs. These associations were independent of rate- or rhythm-controlling drugs.