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Background and Aims Standardized definitions for outcome measures in randomized clinical trials and observational studies are essential for robust and valid evaluation of medical products, interventions, care, and outcomes. The European Unified Registries for Heart Care Evaluation and Randomised Trials (EuroHeart) project of the European Society of Cardiology aimed to create international data standards for cardiovascular clinical study outcome measures. Methods The EuroHeart methods for data standard development were used. From a Global Cardiovascular Outcomes Consortium of 82 experts, five Working Groups were formed to identify and define key outcome measures for: cardiovascular disease (generic outcomes), acute coronary syndrome and percutaneous coronary intervention (ACS/PCI), atrial fibrillation (AF), heart failure (HF) and transcatheter aortic valve implantation (TAVI). A systematic review of the literature informed a modified Delphi method to reach consensus on a final set of variables. For each variable, the Working Group provided a definition and categorized the variable as mandatory (Level 1) or optional (Level 2) based on its clinical importance and feasibility. Results Across the five domains, 24 Level 1 (generic: 5, ACS/PCI: 8, AF: 2; HF: 5, TAVI: 4) and 48 Level 2 (generic: 18, ACS-PCI: 7, AF: 6, HF: 2, TAVI: 15) outcome measures were defined. Conclusions Internationally derived and endorsed definitions for outcome measures for a range of common cardiovascular diseases and interventions are presented. These may be used for data alignment to enable high-quality observational and randomized clinical research, audit, and quality improvement for patient benefit. [ABSTRACT FROM AUTHOR]

Atherosclerotic cardiovascular disease (ASCVD) and consequent acute coronary syndromes (ACS) are substantial contributors to morbidity and mortality across Europe. Fortunately, as much as two thirds of this disease's burden is modifiable, in particular by lipid-lowering therapy (LLT). Current guidelines are based on the sound premise that, with respect to low-density lipoprotein cholesterol (LDL-C), "lower is better for longer", and recent data have strongly emphasised the need for also "the earlier the better". In addition to statins, which have been available for several decades, ezetimibe, bempedoic acid (also as fixed dose combinations), and modulators of proprotein convertase subtilisin/kexin type 9 (PCSK9 inhibitors and inclisiran) are additionally very effective approaches to LLT, especially for those at very high and extremely high cardiovascular risk. In real life, however, clinical practice goals are still not met in a substantial proportion of patients (even in 70%). However, with the options we have available, we should render lipid disorders a rare disease. In April 2021, the International Lipid Expert Panel (ILEP) published its first position paper on the optimal use of LLT in post-ACS patients, which complemented the existing guidelines on the management of lipids in patients following ACS, which defined a group of "extremely high-risk" individuals and outlined scenarios where upfront combination therapy should be considered to improve access and adherence to LLT and, consequently, the therapy's effectiveness. These updated recommendations build on the previous work, considering developments in the evidential underpinning of combination LLT, ongoing education on the role of lipid disorder therapy, and changes in the availability of lipid-lowering drugs. Our aim is to provide a guide to address this unmet clinical need, to provide clear practical advice, whilst acknowledging the need for patient-centred care, and accounting for often large differences in the availability of LLTs between countries. [ABSTRACT FROM AUTHOR]

Introduction: Atrial fibrillation (AF) and heart failure (HF) often coexist due to the common elements of the pathomechanism they share. The potential significance of the order these entities present in the same patient is ill-defined. Herein, we report our results from a nationwide database on the occurrence of various sequences AF and HF may present, the time delays between the two conditions and all-cause mortality associated with different scenarios. Methods: Patients diagnosed with both AF and HF between 2015 and 2021 were enrolled from the Hungarian National Health Insurance Fund (NHIF) database. The order the two entities followed each other, and the time delay in between were registered. Median survival rates were calculated in AF → HF; HF → AF and simultaneous scenarios. Results: A total of 109,075 patients were enrolled: 29,937 with AF → HF, 38,171 with HF → AF, and 40,967 diagnosed simultaneously. Time delays between AF → HF and HF → AF were 6 and 10 months, respectively. The median survival was 46 months in the AF → HF, 38 months in the HF → AF, and 21 months in the simultaneous group. Patients with HF → AF, and with simultaneous presentations had 5% and 16% greater mortality risk as compared to the AF → HF sequence, with hazard ratios (95% confidence intervals) of 0.95 (0.93–0.97) and 0.84 (0.82–0.85), respectively (P < 0.0001). Conclusions: HF occurred significantly earlier after the diagnosis of AF than vice versa. Patients diagnosed simultaneously had the worst, while the AF → HF sequence had the best prognosis. These data should have implications for the intensification of monitoring and therapy in different scenarios. [ABSTRACT FROM AUTHOR]

Aims: The aim of the study was to assess the incidence and predictive factors of the development of heart failure with improved ejection fraction (HFimpEF) category during a 1 year follow‐up period in a heart failure with reduced ejection fraction (HFrEF) patient population managed in a heart failure outpatient clinic. Methods and results: The study evaluated data from patients enrolled in the Hungarian Heart Failure Registry (HHFR). The incidence and predictive factors of the development of the HFimpEF category after 1 year follow‐up were assessed in the group of patients who had HFrEF at baseline. We evaluated the incidence and predictors of the development of HFimpEF after a 1 year follow‐up in relation to time since diagnosis of HFrEF in patients diagnosed within 3 months, between 3 months and 1 year, and beyond 1 year. The predictive factors of the development of HFimpEF were analysed using univariate and multivariate logistic regression analysis. Of the 833 HFrEF patients enrolled in the HHFR, the development of HFimpEF was observed in 162 patients (19.5%) during 1 year follow‐up. In the whole patient population, independent predictors of the development of HFimpEF were female gender [odds ratio (OR): 1.73; 95% confidence interval (CI): 1.01–2.96; P < 0.05], non‐ischaemic aetiology (OR: 1.95; 95% CI: 1.15–3.30; P < 0.05), and left ventricular end‐diastolic diameter (LVEDD) <60 mm (OR: 2.04; 95% CI: 1.18–3.51; P < 0.05). The 1 year incidence of HFimpEF decreased in relation to time since diagnosis of HFrEF. The incidence of HFimpEF was 27.1% in patients diagnosed within 3 months, 18.4% in patients diagnosed between 3 months and 1 year, and 12.2% in patients diagnosed beyond 1 year. Non‐ischaemic aetiology (OR: 4.76; 95% CI: 1.83–12.4; P < 0.01) and QRS width (OR: 0.81; 95% CI: 0.71–0.94; P < 0.01) for patients diagnosed within 3 months, LVEDD (OR: 0.54; 95% CI: 0.32–0.90; P < 0.05) and left atrial diameter ≤45 mm (OR: 5.44; 95% CI: 1.45–20.4; P < 0.05) for patients diagnosed between 3 months and 1 year, and LVEDD < 67 mm (OR: 2.71; 95% CI: 1.07–6.88; P < 0.05) for patients diagnosed beyond 1 year were found to be independent predictive factors. Conclusions: In our study, in this HFrEF patient population managed in a heart failure outpatient clinic, the 1 year incidence of HFimpEF was found to be ~20%. The 1 year incidence of HFimpEF decreased in relation to time since diagnosis of HFrEF. The most important predictors of the development of HFimpEF were female sex, non‐ischaemic aetiology, narrower QRS width, and smaller diameter of the left ventricle and left atrium. [ABSTRACT FROM AUTHOR]

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Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background and Purpose: The screening tool for diagnosing lower extremity arterial disease is the assessment of the ankle-brachial index (ABI), which is widely used in general practice. However, resting ABI can easily produce a false negative result. In light of this, our goal was to determine the proportion of definitive diagnoses (peripheral arterial disease [PAD] confirmed or refuted) among patients screened in general practice, and the rate of cases in which the need for further specialized examination is necessary, with special attention to groups having non-compressible arteries and ABI negative symptomatic status. The aim of our work is to improve the efficiency of primary health care screening in PAD and reduce the extremely high domestic amputation ratio.Patients and Methods: Eight hundred and sixteen patients were screened. We used the Edinburgh Questionnaire and recorded medical histories, major risk factors, current complaints, and medication. Physical examinations were performed, including ABI testing.Results: Thirty-three percent complained about lower extremity claudication; 23% had abnormal ABI values; 13% of the patients within the normal ABI range had complaints of dysbasia; and 12% were in the non-compressible artery group. The ABI-negative symptomatic group's risk factor profile showed a close similarity to the clear PAD-positive and non-compressible artery groups.Conclusion: The percentage of PAD could be higher than the number of patients diagnosed by ABI screening. Nearly a quarter of the population fell into the non-compressible artery and ABI-negative symptomatic groups, together defined as the "murky zone". When screening purposely for PAD, these patients deserve special attention due to the insufficient selectivity and sensitivity of measurements. If there is high clinical suspicion of PAD in spite of normal ABI values, further assessment may be considered. [ABSTRACT FROM AUTHOR]

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Hungarian Medical Journal / Orvosi Hetilap is the property of Akademiai Kiado and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Endocannabinoids are among the most intensively studied lipid mediators of cardiovascular functions. In the present study the effects of decreased and increased activity of the endocannabinoid system (achieved by cannabinoid-1 (CB1) receptor blockade and inhibition of cannabinoid reuptake, respectively) on the systemic and cerebral circulation were analyzed under steady-state physiological conditions and during hypoxia and hypercapnia (H/H). Methodology/Principal Findings: In anesthetized spontaneously ventilating rats the CB1-receptor antagonist/inverse agonist AM-251 (10 mg/kg, i.v.) failed to influence blood pressure (BP), cerebrocortical blood flow (CoBF, measured by laser- Doppler flowmetry) or arterial blood gas levels. In contrast, the putative cannabinoid reuptake inhibitor AM-404 (10 mg/kg, i.v.) induced triphasic responses, some of which could be blocked by AM-251. Hypertension during phase I was resistant to AM-251, whereas the concomitant CoBF-increase was attenuated. In contrast, hypotension during phase III was sensitive to AM-251, whereas the concomitant CoBF-decrease was not. Therefore, CoBF autoregulation appeared to shift towards higher BP levels after CB1-blockade. During phase II H/H developed due to respiratory depression, which could be inhibited by AM-251. Interestingly, however, the concomitant rise in CoBF remained unchanged after AM-251, indicating that CB1-blockade potentially enhanced the reactivity of the CoBF to H/H. In accordance with this hypothesis, AM-251 induced a significant enhancement of the CoBF responses during controlled stepwise H/H. Conclusion/Significance: Under resting physiological conditions CB1-receptor mediated mechanisms appear to have limited influence on systemic or cerebral circulation. Enhancement of endocannabinoid levels, however, induces transient CB1-independent hypertension and sustained CB1-mediated hypotension. Furthermore, enhanced endocannabinoid activity results in respiratory depression in a CB1-dependent manner. Finally, our data indicate for the first time the involvement of the endocannabinoid system and CB1-receptors in the regulation of the cerebral circulation during H/H and also raise the possibility of their contribution to the autoregulation of CoBF. [ABSTRACT FROM AUTHOR]

In previous studies, different parameters of arterial stiffness were related to cardiovascular mortality in hemodialysis patients, but their relative prognostic value has not previously been evaluated in 1 cohort. Carotid-femoral pulse wave velocity (PWV), the carotid augmentation index, carotid pulse pressure (CPP) and carotid-brachial pulse pressure amplification (AMP) were measured in 98 patients before and after hemodialysis. Patients were followed for a median of 29 months (1–34) and the association of these parameters with cardiovascular mortality were assessed using log-rank tests and Cox proportional hazards regressions. During follow-up, 25 patients died of cardiovascular causes. Increasing pre- and postdialysis PWV tertiles and decreasing predialysis AMP tertiles were significantly related to cardiovascular mortality (p = 0.012 and 0.011 for PWV, respectively; < 0.001 for AMP). Neither the carotid augmentation index nor carotid pulse pressure were related to cardiovascular mortality. The adjusted hazard ratios for 1 m/s higher pre- and postdialysis PWV were 1.24 (1.07–1.44) and 1.17 (1.06–1.28), respectively. The hazard ratio for 10% lower predialysis AMP was 1.41 (1.03–1.92). When included in the same model, both predialysis PWV and AMP remained significantly associated with cardiovascular mortality. Among different stiffness parameters, PWV is consistently related to cardiovascular mortality, irrespective of the timing of measurement. Predialysis AMP seems to provide additional prognostic information. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Measuring arterial stiffness (augmentation index (AI), aortic pulse wave velocity (PWV)) in hemodialysis (HD) patients has prognostic significance. To assess its validity, the new oscillometric Arteriograph device (AIA, PWVA) was compared to the validated PulsePen tonometer (AIP, PWVP). Methods: AI and PWV were measured in 98 patients with both devices before HD. Validity was evaluated by Pearson’s correlation, Bland-Altman analysis, and by assessing the prognostic value of AI and PWV to predict cardiovascular (CV) mortality over 29 months. Results: Correlation between AIP and AIA was significant (R = 0.527, p < 0.001). The mean difference of AI values obtained by the two devices was –20.6%, and 30% of the paired AI differences fall outside the ±1 SD boundary of the mean between-device difference. There was no significant correlation between the PWVP and PWVA readings (R = 0.173, p = 0.097). The average difference of PWV values by the two devices was –1.2 m/s, and 20.6% of the paired PWV differences fall outside the ±1 SD boundary. In survival analyses, only PWVP but not PWVA was significantly related to CV mortality. Conclusion: Lack of correlation between PWVP and PWVA and lack of prognostic significance of PWVA suggest limited validity of Arteriograph to determine PWV in patients on HD. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Aortic valve calcification (AVC) and carotid artery calcification (CAC) are considered to be markers of generalized atherosclerosis. However, the role of intracardiac calcification (ICC) (valvular and perivalvular calcification) is unclear, The objective of this retrospective study was to analyze the relationship between ICC and CAC, risk factors, and clinical atherosclerotic disease. Risk factors included age, sex, diabetes mellitus, hypercholesterolemia, and hypertension; clinical atherosclerosis comprised stroke, coronary artery disease, and peripheral artery disease. Between January 1, 2001, and January 1, 2004, all consecutive patients were enrolled into the study who underwent both carotid ultrasonography and transthoracic echocardiography examinations within 2 months, Patients with renal failure, substantial aortic stenosis, and carotid artery occlusion were excluded. There were 320 patients (104 men; mean ± SEM age, 66.6 ± 0.76 years). Positive results on carotid ultrasonography are defined as any CAC. Patients were categorized as having mild, moderate, or severe CAC. Positive results on transthoracic echocardiography were defined as any ICC; AVC was defined as mitral anulus calcification (MAC) or both. Intracardiac calcification was found in 181 patients, AVC in 51 patients, MAC in 48 patients, and calcification of both structures in 82 patients. Using multiple logistic regression analysis, ICC (odds ratio, 1.9), age (10-year periods) (odds ratio, 2.0), and the presence of peripheral artery disease (odds ratio, 1.7) were independent predictors of CAC. Carotid ultrasonography results were positive in 227 patients. For CAC, the sensitivities of AVC, MAC, both, and any ICC were 52.4%, 52.0%, 33.5%, and 7 1.2%, respectively, and the specificities were 84.9%, 87.1%, 92.5%, and 78.5%, respectively. The extension of ICC as 0, 1 location (AVC or MAC) , or 2 locations (AVC and MAC) was associated with the severity of CAC (P < .00 1, τ = 0.42). There was no difference between patients with AVC vs patients with MAC in the presence of different stages of CAC (P = .62). Intracardiac calcification (MAC or AVC) is an independent predictor of CAC as a marker of atherosclerosis, although the lack of ICC does not rule out atherosclerosis. Intracardiac calcification is related to CAC, with high specificity. The extension of ICC is related to the severity of atherosclerosis. Based on our results, antiatherothrombotic therapy should be considered in patients with ICC even before obtaining a positive carotid ultrasonography result. [ABSTRACT FROM AUTHOR]

Endocannabinoids and CB 1 receptors have been implicated in endotoxin (LPS)-induced hypotension: LPS stimulates the synthesis of anandamide in macrophages, and the CB1 antagonist SR-141716 inhibits the hypotension induced by treatment of rats with LPS or LPS-treated macrophages. Recent evidence indicates the existence of cannabinoid receptors distinct from CB 1 or CB2 that are inhibited by SR-141716 but not by other CB 1 antagonists such as AM251. In pentobarbitalanesthetized rats, intravenous injection of 10 mg/kg LPS elicited hypotension associated with profound decreases in cardiac contractility, moderate tachycardia, and an increase in lower body vascular resistance. Pretreatment with 3 mg/kg SR-141716 prevented the hypotension and decrease in cardiac contractility, slightly attenuated the increase in peripheral resistance, and had no effect on the tachycardia caused by LPS, whereas pretreatment with 3 mg/kg AM251 did not affect any of these responses. SR-141716 also elicited an acute reversal of the hypotension and decreased contractility when administered after the response to LPS had fully developed. The LPS induced hypotension and its inhibition by SR-141716 were similar in pentobarbital-anesthetized wild-type, CB1-/-, and CB1-/-/CB2-/- mice. We conclude that SR-141716 inhibits the acute hemodynamic effects of LPS by interacting with a cardiac receptor distinct from CB 1 or CB2 that mediates negative inotropy and may be activated by anandamide or a related endocannabinoid released during endotoxemia. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction is detectable both in the forearm skin microcirculation by laser Doppler flowmetry and in the brachial artery by Duplex Ultrasound. The aim of the study was to evaluate whether endothelium-dependent vasodilation in the forearm micro circulation is related to endothelium-dependent flow mediated dilation (FMD) of the brachial artery. In 22 treated male essential hypertensive patients (EHT) who had impaired FMD of the brachial artery, and in 11 male normotensive subjects (NT) we measured first the postocclusive reactive hyperemic response (PORH), then the effect of two doses of acetylcholine (ACh) and sodium nitroprusside (SNP) on the forearm skin micro circulation. FMD resulted from forearm reactive hyperemia induced by 5 minutes of ischaemia and the vasodilation induced by sublingual nitroglycerine (GTN) were also measured. Responses were calculated as the maximal percent increase above baseline. PORH and the responses to ACh were significantly (p < 0.05, p < 0.01) reduced in EHT (272 ± 180, 177 ± 194, 463 ± 302) as compared to NT (409 ± 123, 470 ± 467, 805 ± 603). Response to SNP was similar. FMD was significantly (p < 0.001) reduced in EHT as compared to NT (3.98 ± 2.2 vs 9.3 ± 2.88), while response to GTN was similar. There was no significant relationship (p = n.s.) either between maximal response to ACh and FMD (r = 0.28), or between PORH and FMD (r = -0.01). Endothelial dysfunction was detectable with both methods in EHT. Our results show that endothelium-dependent vasodilation in forearm microcirculation is not related to FMD of the brachial artery. This can be explained by the differences in vascular beds and mechanism involved in the hyperemic response. [ABSTRACT FROM AUTHOR]

Advanced cirrhosis is associated with generalized vasodilation of unknown origin, which contributes to mortality. Cirrhotic patients are endotoxemic, and activation of vascular cannabinoid CB1 receptors has been implicated in endotoxin-induced hypotension. Here we show that rats with biliary cirrhosis have low blood pressure, which is elevated by the CB1 receptor antagonist SR141716A. The low blood pressure of rats with CCl4-induced cirrhosis was similarly reversed by SR141716A, which also reduced the elevated mesenteric blood flow and portal pressure. Monocytes from cirrhotic but not control patients or rats elicited SR141716A-sensitive hypotension in normal recipient rats and showed significantly elevated levels of anandamide. Compared with non-cirrhotic controls, in cirrhotic human livers there was a three-fold increase in CB1 receptors on isolated vascular endothelial cells. These results implicate anandamide and vascular CB1 receptors in the vasodilated state in advanced cirrhosis and indicate a novel approach for its management. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor regarding cannabinoids and endotoxemia, featured in a previous issue of the "American Journal of Physiology: Heart Circulatory Physiology."