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Background: Heart failure due to high cardiac output rarely occurs. Few cases of post-traumatic arteriovenous fistula (AVF) as a cause of high-output failure were reported in the literature. Methods: Herein, we report a case of 33-year-old male who was admitted to our institution due to symptoms of heart failure. He reported a gunshot injury of the left thigh 4 months earlier, when he had been shortly hospitalized and discharged 4 days later. Since the gunshot injury he had exertional dyspnea and left leg edema, so the diagnostic procedures were performed. Results: Clinical examination revealed distended neck veins, tachycardia, slightly palpable liver, left leg edema, and thrill over the left thigh. Due to high clinical suspicion, duplex ultrasonography of the left leg was performed that verified femoral AVF. Operative treatment of AVF was made with prompt resolution of symptoms. Conclusions: This case wants to emphasize the importance of proper clinical examination, and duplex ultrasonography in all cases of penetrating injuries. [ABSTRACT FROM AUTHOR]

Background A coronary artery aneurysm is a rare cardiac anomaly that may be incidentally detected on echocardiography. When associated with a coronary cameral fistula, an aneurysm can become symptomatic. We present a unique case of a giant left circumflex coronary aneurysm with a fistula to the left atrium and a large atrial septal defect causing acute heart failure in a young woman during the peripartum period. Case summary A 32 year-old woman who presented with hypoxia after the delivery of her fourth child was found to have heart failure with severe mitral regurgitation and multiple abnormal intracardiac shunts. Echocardiography showed a large circular structure with Doppler color flow into the left atrium and between the atria. Cardiac computed tomography showed multiple dilated coronary arteries including a left circumflex coronary artery aneurysm measuring >10 cm in diameter with fistulous communication to the left atrium and a large atrial septal defect. A right heart catheterization was performed, and the patient was diagnosed with high-output heart failure. Surgical closure of the coronary cameral fistula was deferred due to the risk of worsening pressure in the coronary aneurysm, and the patient was referred for cardiac transplantation. Discussion This case illustrates severe heart failure as a complication of a giant coronary artery aneurysm with fistulization to the left atrium and subsequent shunting through a large atrial defect. Echocardiography allows for the detection of a coronary aneurysm and shunting, and cardiac computed tomography provides detailed visualization of a coronary cameral fistula. [ABSTRACT FROM AUTHOR]

We introduce the innovative use of technetium-99m–labeled macroaggregated albumin to diagnose high-output heart failure in a patient with multiple myeloma with persistent congestion symptoms. Symptom resolution occurred with lenalidomide and steroids. This marks the first clinical use of technetium-99m–labeled macroaggregated albumin for clarifying high-output heart failure etiology.

BackgroundHepatic arteriovenous malformations (AVMs) in hereditary hemorrhagic telangiectasia (HHT) patients are most commonly hepatic artery to hepatic venous shunts which can result in high-output heart failure. This condition can be debilitating and is a leading cause of liver transplantation in HHT patients. However, it is not known what characteristics can discriminate between asymptomatic patients and those who will develop heart failure symptoms.Results176 patients with HHT were evaluated with computed tomography angiography (CTA) between April 2004 and February 2019 at our HHT Center of Excellence. 63/176 (35.8%) patients were found to have hepatic AVMs on CTA. 18 of these patients were excluded because of the presence of another condition which could confound evaluation of heart failure symptoms. In the remaining 45 patients included in our cohort, 25/45 (55.6%) patients were classified as asymptomatic and 20/45 (44.4%) were classified as symptomatic, and these groups were compared. In symptomatic patients, mean common hepatic artery (CHA) diameter was significantly higher (11.1 versus 8.4 mm) and mean hemoglobin levels were significantly lower (10.7 vs 12.6 g/dL). A stepwise multiple logistic regression analysis demonstrated that both CHA diameter and hemoglobin level were independent predictors of heart failure symptoms with ORs of 2.554 (95% CI 1.372-4.754) and 0.489 (95% CI 0.299-0.799), respectively. The receiver operator characteristic (ROC) curve of our analysis demonstrated an AUC of 0.906 (95% CI 0.816-0.996), sensitivity 80.0% (95% CI 55.7-93.4%), and specificity 75.0% (95% CI 52.9-89.4%).ConclusionsCTA is an effective and easily reproducible method to evaluate hepatic involvement of HHT. Utilizing CTA, clinical, and laboratory data we determined CHA diameter and hemoglobin level were independent predictors of heart failure symptoms.

Abstract Wet beriberi is a rare but fatal disease in modern society. The nonspecific clinical manifestations, including symptoms of heart failure and recalcitrant lactic acidosis, can prevent timely diagnosis. The use of a pulmonary artery catheter can promptly confirm a high cardiac output state and plays a crucial role in rapidly deteriorating cases. Appropriate treatment with intravenous administration of thiamine leads to dramatic recovery within hours. We present two cases of Shoshin beriberi, a fulminant variant of wet beriberi, diagnosed in 2016 and 2022 at our institute. The patients experienced haemodynamic collapse and refractory lactic acidosis, which were successfully diagnosed with the use of a pulmonary artery catheter and reversed by thiamine supplementation. We also reviewed 19 cases of wet beriberi reported between 2010 and 2022.

A minority of patients with heart failure present in a high-output state. We described an uncommon case of high-output heart failure caused by an iliac arteriovenous fistula (IAVF), a rare but serious complication after lumbar discectomy surgery (LDS). A 44-year-old man with no notable medical condition except a history of herniated nucleus pulposus necessitating the L4-L5 LDS 5 years ago presented with clinical signs of progressive high-output heart failure. Physical examination revealed wide pulse pressure with bruit and systolic thrill at the right inguinal region. Computed tomographic angiography confirmed the IAVF from the right common iliac artery to the left common iliac vein. There was a significant shunting to the venous system, causing severe dilatation of the inferior vena cava. Notably, the preoperative lumbar magnetic resonance imaging performed 5 years ago demonstrated that the herniated disc was located at the L4-L5 level, which corresponded to the location of IAVF. The patient successfully underwent endovascular closure by covered stent leading to the gradual resolution of symptoms and hemodynamic parameters. Although vascular complications from the LDS are very uncommon, most patients develop severe symptoms from worsening high-output heart failure. This case highlights the essence of careful history taking, physical examinations, and appropriate investigations in guiding the diagnosis and contemplating the treatment strategy.

Hereditary hemorrhagic telangiectasia (HHT) is a rare autosomal dominant hereditary disorder characterized by recurrent spontaneous epistaxis, mucocutaneous telangiectasias, and solid organ arteriovenous malformations (AVMs). Pulmonary hypertension (PH) is an increasingly recognized complication in patients with HHT, most often precipitated by high-output heart failure in the presence of hepatic AVMs as well as pulmonary arterial hypertension in the form of a proliferative vasculopathy. The presence of PH in patients with HHT is associated with significant elevations in rates of morbidity and mortality. Additionally, there is growing recognition of a thromboembolic propensity in this population that increases the risk of chronic thromboembolic PH, posing unique clinical considerations regarding the use of anticoagulation. Patients with HHT are also at risk of PH due to disorders commonly seen in the general population, including left-sided heart and lung disease. The etiology of PH in HHT is multifaceted and complex; the diagnostic approach and treatment strategies must consider the underlying pathophysiology of HHT. This comprehensive review summarizes current knowledge of PH in HHT, detailing the pathogenesis of known etiologies, diagnostic evaluation, and suggested treatment modalities as well as emerging therapies that may be of future interest. [ABSTRACT FROM AUTHOR]

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• A PAVM was diagnosed in a critically ill cyanotic neonate. • Echocardiography played a pivotal role in establishing the diagnosis. • Urgent transcatheter device occlusion resulted in immediate hemodynamic stabilization.

Abstract Hereditary hemorrhagic telangiectasia (HHT) is a rare autosomal dominant hereditary disorder characterized by recurrent spontaneous epistaxis, mucocutaneous telangiectasias, and solid organ arteriovenous malformations (AVMs). Pulmonary hypertension (PH) is an increasingly recognized complication in patients with HHT, most often precipitated by high‐output heart failure in the presence of hepatic AVMs as well as pulmonary arterial hypertension in the form of a proliferative vasculopathy. The presence of PH in patients with HHT is associated with significant elevations in rates of morbidity and mortality. Additionally, there is growing recognition of a thromboembolic propensity in this population that increases the risk of chronic thromboembolic PH, posing unique clinical considerations regarding the use of anticoagulation. Patients with HHT are also at risk of PH due to disorders commonly seen in the general population, including left‐sided heart and lung disease. The etiology of PH in HHT is multifaceted and complex; the diagnostic approach and treatment strategies must consider the underlying pathophysiology of HHT. This comprehensive review summarizes current knowledge of PH in HHT, detailing the pathogenesis of known etiologies, diagnostic evaluation, and suggested treatment modalities as well as emerging therapies that may be of future interest.

Wet beriberi is a rare but fatal disease in modern society. The nonspecific clinical manifestations, including symptoms of heart failure and recalcitrant lactic acidosis, can prevent timely diagnosis. The use of a pulmonary artery catheter can promptly confirm a high cardiac output state and plays a crucial role in rapidly deteriorating cases. Appropriate treatment with intravenous administration of thiamine leads to dramatic recovery within hours. We present two cases of Shoshin beriberi, a fulminant variant of wet beriberi, diagnosed in 2016 and 2022 at our institute. The patients experienced haemodynamic collapse and refractory lactic acidosis, which were successfully diagnosed with the use of a pulmonary artery catheter and reversed by thiamine supplementation. We also reviewed 19 cases of wet beriberi reported between 2010 and 2022. [ABSTRACT FROM AUTHOR]

Background High-output heart failure (HF) is a form of HF where patients present with a high-output state with low systemic vascular resistance. This report presents the case of high-output HF in a patient with an arteriovenous shunt and no options for oral-administered drugs. Case summary A 70-year-old male with a terminal jejunostomy fully depending on parenteral feeding through a vena saphena magna shunt presented with symptoms of shortness of breath. Echocardiography revealed eccentric hypertrophy with reduced left ventricular ejection fraction (LVEF) and atrial fibrillation with a heart rate of 70–100 b.p.m. Cardiac magnetic resonance imaging, endomyocardial biopsy, and cardiomyopathy lab revealed no cause of HF. High-output HF based on right heart catheterization due to the arteriovenous shunt or related to irregularity due to atrial fibrillation were potential causes. As a result of his malfunctioning gastrointestinal system, the pharmacological options were limited. He was treated with captopril sublingual, initially 6.25 mg three times daily (TID) and later 12.5 mg TID, which reduced blood pressure. Electrical cardioversion to sinus rhythm was successful but did not improve LVEF. Therefore, the patient was opted for surgically reducing the blood flow through the shunt, resulting in normalization of LVEF. Discussion High-output HF is an uncommon form of HF with an uncertain prevalence. The most common aetiologies reported in the literature are obesity, cirrhosis, and arteriovenous shunts. Sublingual administration of captopril can be an effective treatment option for HF patients unable to absorb oral-administered drugs. [ABSTRACT FROM AUTHOR]

Key Clinical Messages: Hereditary hemorrhagic telangiectasia (HHT), a rare hereditary disorder, can cause recurrent massive epistaxis and gastrointestinal bleeding leading to severe anemia. Early diagnosis of HHT is essential to provide timely interventional therapies. HHT is a rare autosomal dominant hereditary disease that results in abnormal vasculogenesis in the skin, mucous membranes, and visceral organs such as the liver, lungs, and brain. Clinical diagnosis of HHT is made using the Curacao criteria, which include recurrent spontaneous nosebleeds, mucocutaneous telangiectasias, visceral organ involvement, and first‐degree family history of HHT. Here, we report a patient with HHT from Ethiopia, who presented with recurrent epistaxis and gastrointestinal bleeding, and severe anemia requiring frequent blood transfusions as well as cauterization. The presented case is a 42‐year‐old Black Ethiopian man with frequent hospitalization for severe anemia and high‐output heart failure requiring frequent blood transfusions. His mother had bilateral epistaxis since her early adulthood. Physical examination was significant for tachycardia, pale conjunctivae, and tiny erythematous lesions over his tongue, ejection systolic murmur and peripheral edema. Laboratory investigations revealed severe anemia with iron deficiency picture. Upper gastrointestinal endoscopy showed multiple telangiectasia spots and abdominal Doppler ultrasound showed hepatic arterio‐venous malformations. He received supportive management and electrocauterization of nasal, gastric, and duodenal telangiectasias. To the best of our knowledge, this is the first case of HHT to be reported from Ethiopia. High degree of suspicion and early diagnosis of HHT is essential to start preventive screening and surveillance and provide timely interventional therapies. HHT can cause recurrent massive epistaxis and gastrointestinal bleeding leading to severe anemia and high‐output heart failure. In resource limited settings, selective cauterization of telangiectasia will help to control bleeding, although it does not avoid recurrent bleeding. [ABSTRACT FROM AUTHOR]

Infantile hepatic hemangioma (IHH) is the most common benign liver tumor in children, and multifocal and diffuse tumors often become life-threatening, necessitating therapy. Propranolol is now considered the first choice of therapy with ample data in Caucasian children. We present a series of nine Indian children with multifocal (n = 5) and diffuse (n = 4) IHH treated with propranolol monotherapy. This was a retrospective clinical data-based single-center study. Propranolol was used at a median dose of 3.2 mg/kg/day (range 3–3.3 mg/kg/day) for a median duration of 12 months (range 6–32 months). The presentations of IHH (either in isolation or combination) were hypothyroidism in six patients (diagnosed by elevated serum TSH levels), heart failure in three (diagnosed based on clinical and echocardiographic features), and imaging evidence of macrovascular shunting in two patients. A good response to propranolol monotherapy (with a median dose of 3.2 mg/kg/day for a median duration of 12 months) was observed in eight patients, with a poor response in one. One patient experienced recurrence but responded adequately to propranolol retreatment. Our data reiterate the excellent response (88.9% responded) and safety profile with propranolol monotherapy in complicated IHH and strengthen the data in Asian (Indian) children. It includes the maximum proportion of complicated IHH treated with propranolol in East and South Asia, and the largest series from India. [Display omitted] [ABSTRACT FROM AUTHOR]

Key Clinical Messages Hereditary hemorrhagic telangiectasia (HHT), a rare hereditary disorder, can cause recurrent massive epistaxis and gastrointestinal bleeding leading to severe anemia. Early diagnosis of HHT is essential to provide timely interventional therapies. Abstract HHT is a rare autosomal dominant hereditary disease that results in abnormal vasculogenesis in the skin, mucous membranes, and visceral organs such as the liver, lungs, and brain. Clinical diagnosis of HHT is made using the Curacao criteria, which include recurrent spontaneous nosebleeds, mucocutaneous telangiectasias, visceral organ involvement, and first‐degree family history of HHT. Here, we report a patient with HHT from Ethiopia, who presented with recurrent epistaxis and gastrointestinal bleeding, and severe anemia requiring frequent blood transfusions as well as cauterization. The presented case is a 42‐year‐old Black Ethiopian man with frequent hospitalization for severe anemia and high‐output heart failure requiring frequent blood transfusions. His mother had bilateral epistaxis since her early adulthood. Physical examination was significant for tachycardia, pale conjunctivae, and tiny erythematous lesions over his tongue, ejection systolic murmur and peripheral edema. Laboratory investigations revealed severe anemia with iron deficiency picture. Upper gastrointestinal endoscopy showed multiple telangiectasia spots and abdominal Doppler ultrasound showed hepatic arterio‐venous malformations. He received supportive management and electrocauterization of nasal, gastric, and duodenal telangiectasias. To the best of our knowledge, this is the first case of HHT to be reported from Ethiopia. High degree of suspicion and early diagnosis of HHT is essential to start preventive screening and surveillance and provide timely interventional therapies. HHT can cause recurrent massive epistaxis and gastrointestinal bleeding leading to severe anemia and high‐output heart failure. In resource limited settings, selective cauterization of telangiectasia will help to control bleeding, although it does not avoid recurrent bleeding.

IntroductionHeart failure (HF) is a serious complication of end-stage kidney disease (ESKD). However, most data come from retrospective studies that included patients on chronic hemodialysis at the time of its initiation. These patients are frequently overhydrated, which significantly influences the echocardiogram findings. The primary aim of this study was to analyze the prevalence of heart failure and its phenotypes. The secondary aims were (1) to describe the potential of N-terminal pro-brain natriuretic peptide (NTproBNP) for HF diagnosis in ESKD patients on hemodialysis, (2) to analyze the frequency of abnormal left ventricular geometry, and (3) to describe the differences between various HF phenotypes in this population.MethodsWe included all patients on chronic hemodialysis for at least 3 months from five hemodialysis units who were willing to participate, had no living kidney transplant donor, and had a life expectancy longer than 6 months at the time of inclusion. Detailed echocardiography together with hemodynamic calculations, dialysis arteriovenous fistula flow volume calculation, and basic lab analysis were performed in conditions of clinical stability. Excess of severe overhydration was excluded by clinical examination and by employing bioimpedance.ResultsA total of 214 patients aged 66.4 ± 14.6 years were included. HF was diagnosed in 57% of them. Among patients with HF, HF with preserved ejection fraction (HFpEF) was, by far, the most common phenotype and occurred in 35%, while HF with reduced ejection fraction (HFrEF) occurred only in 7%, HF with mildly reduced ejection fraction (HFmrEF) in 7%, and high-output HF in 9%. Patients with HFpEF differed from patients with no HF significantly in the following: they were older (62 ± 14 vs. 70 ± 14, p = 0.002) and had a higher left ventricular mass index [96(36) vs. 108(45), p = 0.015], higher left atrial index [33(12) vs. 44(16), p

Abstract Background High-output heart failure is a rare condition that occurs when the heart is unable to respond to a sustained increase in blood demand. On echocardiography, a cardiac index of > 4 L/min/m2 (or 6 L/min) is a clear indicator of this disorder. The causes of high-output heart failure vary, but they all involve peripheral vasodilation or arteriovenous shunting. Renal cell carcinoma is well known for producing high levels of angiogenic growth factors that induce arteriovenous shunts. The decrease in peripheral arterial resistance and the increase in venous return result in a permanent high cardiac output, followed by congestive heart failure. Single bone metastases of renal clear cell carcinoma tumours causing high cardiac output and heart failure symptoms have been reported less than ten times in the medical literature. Case presentation Before a right-shoulder painful lump with a murmur when auscultated, magnetic resonance imaging revealed a large scapular mass, which was biopsied and found to be a bone metastasis of renal cell carcinoma. Two months later, the patient developed heart failure for the first time. There was no evidence of cardiac disease on echocardiography. The cardiac output was 9.8 L/min and the cardiac index was 5.1 L/min/m2. Doppler ultrasound revealed numerous arteriovenous shunts in the large scapular metastasis and a right axillary artery flow of 24% of cardiac output. Sustained lower cardiac output was obtained following lesion-focused radiotherapy and systemic antiangiogenic treatment with axitinib and pembrolizumab. Conclusions Herein, we present a unique case of high-output heart failure in a 70-year-old man diagnosed by echocardiography and upper-limb Doppler ultrasound in the context of metastatic renal cell carcinoma without pre-existing cardiac disease. We stress the potentially life-threatening hemodynamic consequences of hypervascularity associated with arteriovenous shunts within a single metastatic renal cell carcinoma implant, the importance of auscultating any progressing bone mass, and the utility of non-invasive Doppler ultrasound assessment in this setting.

Abstract Background Hepatic arteriovenous malformations (AVMs) in hereditary hemorrhagic telangiectasia (HHT) patients are most commonly hepatic artery to hepatic venous shunts which can result in high-output heart failure. This condition can be debilitating and is a leading cause of liver transplantation in HHT patients. However, it is not known what characteristics can discriminate between asymptomatic patients and those who will develop heart failure symptoms. Results 176 patients with HHT were evaluated with computed tomography angiography (CTA) between April 2004 and February 2019 at our HHT Center of Excellence. 63/176 (35.8%) patients were found to have hepatic AVMs on CTA. 18 of these patients were excluded because of the presence of another condition which could confound evaluation of heart failure symptoms. In the remaining 45 patients included in our cohort, 25/45 (55.6%) patients were classified as asymptomatic and 20/45 (44.4%) were classified as symptomatic, and these groups were compared. In symptomatic patients, mean common hepatic artery (CHA) diameter was significantly higher (11.1 versus 8.4 mm) and mean hemoglobin levels were significantly lower (10.7 vs 12.6 g/dL). A stepwise multiple logistic regression analysis demonstrated that both CHA diameter and hemoglobin level were independent predictors of heart failure symptoms with ORs of 2.554 (95% CI 1.372–4.754) and 0.489 (95% CI 0.299–0.799), respectively. The receiver operator characteristic (ROC) curve of our analysis demonstrated an AUC of 0.906 (95% CI 0.816–0.996), sensitivity 80.0% (95% CI 55.7–93.4%), and specificity 75.0% (95% CI 52.9–89.4%). Conclusions CTA is an effective and easily reproducible method to evaluate hepatic involvement of HHT. Utilizing CTA, clinical, and laboratory data we determined CHA diameter and hemoglobin level were independent predictors of heart failure symptoms.

An autopsy case of Parkes-Weber syndrome presenting high-output heart failure in a patient who died at 52 years old, is reported. The patient had a tumor in the right buttock since childhood, that had grown up to a diameter of 40 cm diameter by the age of 43 years when he felt exertional dyspnea and was diagnosed as having high-output heart failure due to arteriovenous fistulas. Embolotherapy was attempted, which relieved the symptoms. After 4 years his heart failure deteriorated. We performed embolotherapy but his condition did not improve. He died 1.5 years later. The autopsy revealed the weight of the heart was 1040 g with abundant subendocardial and interstitial fibrosis. In this patient, the level of output had been over 16 L/min which lasted for nine years. The left ventricular ejection fraction (LVEF) decreased during the first five years. Each embolotherapy reduced the cardiac output (CO), which was achieved by a large decrease in heart rate (HR) and a small increase in stroke volume (SV) i.e. CO = HR × SV, and was reflected in the increase in LVEF. • Parkes-Weber syndrome has occasionally extensive arteriovenous fistulas in the pelvis that show high-output heart failure. • Treatment of such cases is difficult, but embolotherapy has partial effects on improving hemodynamics. • A long-term high-output state induces interstitial myocardial fibrosis and collagenous subendocardial thickening. [ABSTRACT FROM AUTHOR]

Abstract Background Aortocoronary arteriovenous fistula (ACAVF) due to iatrogenic bypass grafting to a cardiac vein is an exceedingly rare complication resulting from coronary artery bypass grafting (CABG) surgery. If not identified in a timely fashion, ACAVF has known significant clinical consequences related to left to right shunting and possible residual myocardial ischemia. Case presentation An 82-year-old male with a history of CABG, presented with dyspnea. Over the span of 2 years following CABG, the patient experienced progressive exertional dyspnea and peripheral edema. The patient was found to have a new cardiomyopathy with a severely reduced ejection fraction at 30–35%. The patient underwent diagnostic left heart catheterization, and an ACAVF was discovered between a saphenous vein graft and the coronary sinus. The patient underwent successful percutaneous coiling of the ACAVF with no residual flow. Follow-up echocardiography at 3 months revealed restoration of left ventricular systolic function to 50% and significant improvement in heart failure symptoms. Conclusions ACAVF is an exceedingly rare iatrogenic complication of CABG that may result in residual ischemia from the non-grafted myocardial territory and other sequelae relating to left to right shunting and a high-output state. Management for this pathology includes but is not limited to the use of percutaneous coiling, implantation of covered stents, graft removal and regrafting, and ligation.

Abstract Aims High‐flow arteriovenous fistula (AVF) for haemodialysis leads to profound haemodynamic changes and sometimes to heart failure (HF). Cardiac output (CO) is divided between the AVF and body tissues. The term effective CO (COef) represents the difference between CO and AVF flow volume (Qa) and better characterizes the altered haemodynamics that may result in organ hypoxia. We investigated the effects of Qa reduction on systemic haemodynamics and on brain oxygenation. Methods and results This is a single‐centre interventional study. Twenty‐six patients on chronic haemodialysis with high Qa (>1500 mL/min) were indicated for surgical Qa reduction for HF symptoms and/or signs of structural heart disease on echocardiography. The included patients underwent three sets of examinations: at 4 months and then 2 days prior and 6 weeks post‐surgical procedure. Clinical status, echocardiographical haemodynamic assessment, Qa, and brain oximetry were recorded. All parameters remained stable from selection to inclusion. After the procedure, Qa decreased from 3.0 ± 1.4 to 1.3 ± 0.5 L/min, P 2.0 L/min. These observations were mirrored by higher brain oxygenation and might explain HF symptoms and improved haemodynamics even in asymptomatic high Qa patients.

Aims BMP9 and BMP10 mutations were recently identified in patients with pulmonary arterial hypertension, but their specific roles in the pathogenesis of the disease are still unclear. We aimed to study the roles of BMP9 and BMP10 in cardiovascular homeostasis and pulmonary hypertension using transgenic mouse models deficient in Bmp9 and/or Bmp10. Methods and results Single- and double-knockout mice for Bmp9 (constitutive) and/or Bmp10 (tamoxifen inducible) were generated. Single-knock-out (KO) mice developed no obvious age-dependent phenotype when compared with their wild-type littermates. However, combined deficiency in Bmp9 and Bmp10 led to vascular defects resulting in a decrease in peripheral vascular resistance and blood pressure and the progressive development of high-output heart failure and pulmonary hemosiderosis. RNAseq analysis of the lungs of the double-KO mice revealed differential expression of genes involved in inflammation and vascular homeostasis. We next challenged these mice to chronic hypoxia. After 3 weeks of hypoxic exposure, Bmp10 -cKO mice showed an enlarged heart. However, although genetic deletion of Bmp9 in the single- and double-KO mice attenuated the muscularization of pulmonary arterioles induced by chronic hypoxia, we observed no differences in Bmp10- cKO mice. Consistent with these results, endothelin-1 levels were significantly reduced in Bmp9 deficient mice but not Bmp10 -cKO mice. Furthermore, the effects of BMP9 on vasoconstriction were inhibited by bosentan, an endothelin receptor antagonist, in a chick chorioallantoic membrane assay. Conclusions Our data show redundant roles for BMP9 and BMP10 in cardiovascular homeostasis under normoxic conditions (only combined deletion of both Bmp9 and Bmp10 was associated with severe defects) but highlight specific roles under chronic hypoxic conditions. We obtained evidence that BMP9 contributes to chronic hypoxia-induced pulmonary vascular remodelling, whereas BMP10 plays a role in hypoxia-induced cardiac remodelling in mice. [ABSTRACT FROM AUTHOR]

We present a case of a child with high-output heart failure and severe iron deficiency anaemia-induced dilated cardiomyopathy managed with serial blood transfusions, preload and afterload reducing agents, inotropic therapies, and long-term iron supplementation. The complete resolution of echocardiogram findings of moderate enlargement of all cardiac chambers and moderately depressed left ventricular systolic function was achieved.

We introduce the innovative use of technetium-99m-labeled macroaggregated albumin to diagnose high-output heart failure in a patient with multiple myeloma with persistent congestion symptoms. Symptom resolution occurred with lenalidomide and steroids. This marks the first clinical use of technetium-99m-labeled macroaggregated albumin for clarifying high-output heart failure etiology., Competing Interests: The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)

Background: Thiamine deficiency is an uncommon cause of severe illness in the United States that can lead to significant morbidity because of high-output cardiac failure, peripheral neuropathy, and permanent neurologic impairment. We report the case of a middle-aged woman with extreme malnutrition caused by complications of Roux-en-Y gastric bypass (RYGB) surgery who presented with signs and symptoms of severe thiamine deficiency and septic shock.Case Report: A 43-year-old woman who had undergone RYGB surgery and who had multiple complications presented to the emergency department with agitation, confusion, and lethargy. The physical examination revealed an obtunded woman appearing much older than her reported age with significant peripheral edema. She was hypoxemic, hypotensive, and febrile. The initial laboratory analysis revealed a serum lactate level above the measurable limit, a normal thyroid-stimulating hormone, and elevated levels of troponin and brain natriuretic peptide. A transthoracic echocardiogram showed high-output heart failure. The patient's family later revealed that for the past year her diet had consisted almost exclusively of frozen blended lattes. High doses of thiamine and folate were started. Her shock, hyperlactatemia, and respiratory failure resolved by hospital day 3 and her encephalopathy resolved soon thereafter. Why Should an Emergency Physician be Aware of This?: Thiamine deficiency is a rare but reversible cause of shock, heart failure, and encephalopathy. Identifying patients who are at risk for severe nutritional deficiencies may aid in more rapid treatment with relatively benign medications with little downside, in this case high-dose vitamin B1, and ultimately improve patient-oriented outcomes such as mortality, morbidity, and hospital length of stay. [ABSTRACT FROM AUTHOR]

Background Primary plasma cell leukaemia is rarely associated with high-output heart failure, and the underlying mechanism is not well understood. We encountered a rare case of high-output heart failure caused by primary plasma cell leukaemia. Its underlying mechanism was clarified through imaging studies. Case summary A 49-year-old man with no specific medical history was admitted to our hospital because of heart failure that did not improve with diuretic therapy. His condition was diagnosed as high-output heart failure and primary plasma cell leukaemia after admission. Extensive bone involvement in primary plasma cell leukaemia and arteriovenous shunts in the same lesion were suspected after various imaging studies. The first cycle of chemotherapy with bortezomib, adriamycin, and dexamethasone led to remission of primary plasma cell leukaemia and improved heart failure symptoms. The patient received further chemotherapy in addition to autologous peripheral blood stem cell transplantation and maintenance therapy and had no recurrence of pPCL or heart failure for 1 year to date. Discussion Primary plasma cell leukaemia can be associated with high-output heart failure, which is caused by arteriovenous shunting at the lesion site with diffuse bone involvement. Imaging studies may lead to the early diagnosis of aetiology and treatment of patients with high-output heart failure associated with primary plasma cell leukaemia. [ABSTRACT FROM AUTHOR]

Background: Aortocoronary arteriovenous fistula (ACAVF) due to iatrogenic bypass grafting to a cardiac vein is an exceedingly rare complication resulting from coronary artery bypass grafting (CABG) surgery. If not identified in a timely fashion, ACAVF has known significant clinical consequences related to left to right shunting and possible residual myocardial ischemia. Case presentation: An 82-year-old male with a history of CABG, presented with dyspnea. Over the span of 2 years following CABG, the patient experienced progressive exertional dyspnea and peripheral edema. The patient was found to have a new cardiomyopathy with a severely reduced ejection fraction at 30–35%. The patient underwent diagnostic left heart catheterization, and an ACAVF was discovered between a saphenous vein graft and the coronary sinus. The patient underwent successful percutaneous coiling of the ACAVF with no residual flow. Follow-up echocardiography at 3 months revealed restoration of left ventricular systolic function to 50% and significant improvement in heart failure symptoms. Conclusions: ACAVF is an exceedingly rare iatrogenic complication of CABG that may result in residual ischemia from the non-grafted myocardial territory and other sequelae relating to left to right shunting and a high-output state. Management for this pathology includes but is not limited to the use of percutaneous coiling, implantation of covered stents, graft removal and regrafting, and ligation. [ABSTRACT FROM AUTHOR]

Patients on chronic haemodialysis have a wide range of changes in cardiac function and structure, including left ventricular hypertrophy, dilation and diastolic dysfunction or pulmonary hypertension. All these changes were linked to increased mortality in previous studies. High-flow arteriovenous fistulas (AVF) are supposed to be a factor contributing to their development. This study investigated the early effect of surgical AVF blood flow (Qa) reduction on these changes in patients with or without heart failure changes. Forty-two patients in chronic haemodialysis programme with high-flow AVF (Qa over 1500 mL/min), indicated for surgery for ≥1 of the following indications: 1.manifest heart failure; 2.hand ischemia; 3.advanced structural heart changes detected by echocardiography. The patients underwent echocardiography on selection visit, before blood flow reducing surgery and six weeks thereafter. The Qa reduction led to decrease of left ventricular mass (p = 0.02), end-diastolic volume (p = 0.008), end-diastolic diameter (p = 0.003) and left atrial volume (p = 0.0006). Diastolic function improved. Similarly, right ventricular diameter and right atrial volume decreased (p = 0.000001 and 0.00009, respectively) together with the decrease of estimated pulmonary artery systolic pressure. 81% of patients suffered from pulmonary hypertension prior to surgery, only 36% thereafter. The surgical restriction of the hyperkinetic circulation leads to several improvements of heart structure and function, which was linked to higher mortality in other studies. The beneficial effect of Qa reduction is present even in patients without symptoms of heart failure. The contribution of AVF must be considered with structural or functional heart changes. • Reduction of arteriovenous fistula blood flow leads to decrease of volumes of all heart cavities. • Prognostically significant echocardiographic findings improve after the procedure. • Even the asymptomatic patients benefit from reduction of hyperkinetic circulation. [ABSTRACT FROM AUTHOR]

Aims: High‐flow arteriovenous fistula (AVF) for haemodialysis leads to profound haemodynamic changes and sometimes to heart failure (HF). Cardiac output (CO) is divided between the AVF and body tissues. The term effective CO (COef) represents the difference between CO and AVF flow volume (Qa) and better characterizes the altered haemodynamics that may result in organ hypoxia. We investigated the effects of Qa reduction on systemic haemodynamics and on brain oxygenation. Methods and results: This is a single‐centre interventional study. Twenty‐six patients on chronic haemodialysis with high Qa (>1500 mL/min) were indicated for surgical Qa reduction for HF symptoms and/or signs of structural heart disease on echocardiography. The included patients underwent three sets of examinations: at 4 months and then 2 days prior and 6 weeks post‐surgical procedure. Clinical status, echocardiographical haemodynamic assessment, Qa, and brain oximetry were recorded. All parameters remained stable from selection to inclusion. After the procedure, Qa decreased from 3.0 ± 1.4 to 1.3 ± 0.5 L/min, P < 0.00001, CO from 7.8 ± 1.9 to 6.6 ± 1.5 L/min, P = 0.0002, but COef increased from 4.6 ± 1.4 to 5.3 ± 1.4 L/min, P = 0.036. Brain tissue oxygen saturation increased from 56 ± 11% to 60 ± 9%, P = 0.001. Conclusions: Qa reduction led to increased COef. This was explained by a decreased proportion of CO running through the AVF in patients with Qa > 2.0 L/min. These observations were mirrored by higher brain oxygenation and might explain HF symptoms and improved haemodynamics even in asymptomatic high Qa patients. [ABSTRACT FROM AUTHOR]

Purpose of Review: To provide an overview of the potential iatrogenic causes of acute decompensated heart failure (AHF) and an evidence-based management strategy to address this. Recent Findings: As the heart failure (HF) population continues to age and become burdened with greater comorbidities and polypharmacy, patients become more susceptible to the iatrogenic precipitants of HF. The following clinical scenarios are familiar to clinicians, but the sequelae to AHF are often unanticipated: HF medications withdrawn during an intercurrent illness and not restarted, cardiotoxic therapy prescribed for cancer without timely and regular monitoring of left ventricular function, excessive intravenous fluids administered for sepsis or postoperatively, a blood transfusion volume not adjusted for body weight, iatrogenic anaemia that goes unnoticed or an inappropriate type of pacemaker implanted in a patient with underlying left ventricular systolic dysfunction. Summary: Iatrogenic decompensated HF is a phenomenon that is infrequently documented in the literature but increasingly confronted by clinicians of all specialties. It is associated with a high mortality and morbidity rate. By having greater awareness of these triggers, iatrogenic AHF should be one that is prevented rather than managed when it occurs. [ABSTRACT FROM AUTHOR]

Dramatic cardiomegaly arising from gain-of-function (GoF) mutations in the ATP-sensitive potassium (KATP) channels genes, ABCC9 and KCNJ8, is a characteristic feature of Cantú syndrome (CS). How potassium channel over-activity results in cardiac hypertrophy, as well as the long-term consequences of cardiovascular remodeling in CS, is unknown. Using genome-edited mouse models of CS, we therefore sought to dissect the pathophysiological mechanisms linking KATP channel GoF to cardiac remodeling. We demonstrate that chronic reduction of systemic vascular resistance in CS is accompanied by elevated renin- angiotensin signaling, which drives cardiac enlargement and blood volume expansion. Cardiac enlargement in CS results in elevation of basal cardiac output, which is preserved in aging. However, the cardiac remodeling includes altered gene expression patterns that are associated with pathological hypertrophy and are accompanied by decreased exercise tolerance, suggestive of reduced cardiac reserve. Our results identify a high-output cardiac hypertrophy phenotype in CS which is etiologically and mechanistically distinct from other myocardial hypertrophies, and which exhibits key features of high-output heart failure (HOHF). We propose that CS is a genetically-defined HOHF disorder and that decreased vascular smooth muscle excitability is a novel mechanism for HOHF pathogenesis. [ABSTRACT FROM AUTHOR]

Objective: Chronic intermittent renal replacement therapy(RRT) is an alternate method of decongestion for patients presenting with diuretic-resistant, end-stage heart failure(HF) and cardiorenal syndrome. The optimal method of vascular access has not been confirmed. This study investigated the 6-month outcomes of patients with end-stage HF after the creation of arteriovenous communications (AVC) compared with other means of RRT. Methods: We treated 40 patients with chronic, intermittent, ambulatory RRT, of whom 15 (37.5%; Group A) underwent creation of AVC, and 25 (62.5%; Group B) received intraperitoneal (n=6) or internal jugular catheters (n=19) with the goal of achieving body weight stabilization and relief from congestion. Results: The characteristics of the two groups were similar. According to Cox regression analysis, the 6-month rate of death or re-hospitalization for HF was significantly higher in Group A (73%) than in Group B (44%); hazard ratio (HR): 2.58; 95% confidence interval (CI) 1.2-6.2; P=0.02. Over a 6-month follow-up, the cumulative survival was significantly shorter (P=0.03) in Group A (13.8±10 weeks) than in Group B (20.7±7 weeks). In the 15 patients who received AVC, the only independent predictor of adverse outcome at 6 months was serum total bilirubin concentration (HR 2.5; 95% CI 1.1-5.7, p=0.02), whereas in the 25 patients who underwent other means of RRT, pulmonary vascular resistance (PVR) was identified as a risk factor for hospitalization or death at 1-year follow-up (HR 1.26; 95% CI 1.1-1.57, p=0.04). Conclusion: In patients with end-stage HF, the creation of AVC for intermittent RRT was followed by a significant increase in morbidity and mortality in comparison to the safe and effective placement of permanent central venous catheters. Patients with elevated PVR seem to comprise a group at high risk for adverse outcomes after central catheter insertion.

Abstract Intra-cardiac shunt diseases may cause chronic ventricular volume overload, but extra-cardiac fistula could also cause high-output heart failure (HF). A patient presented with high-output HF and significant extra-cardiac shunt flow. Although the size and shape of the patient's left ventricle suggested dilated cardiomyopathy, considerable origins were not identified except for a high-flow fistula between the right subclavian artery and right internal jugular vein. Right heart catheter examination revealed inappropriately high cardiac output. Left-to-right shunt ratio was calculated at 40.3% from an oximetry run, under the assumption that the left anonymous vein which was not contaminated with any shunt flow could be substituted for venous return from the upper body. We could determine the indication of fistula closure according to the estimated high left-to-right shunt ratio, reducing cardiac output by 42.7% which was similar to the pre-estimated left-to-right shunt ratio. Two months later, the patient's serum B-type natriuretic peptide level and left ventricular end-diastolic and end-systolic diameters were decreased. The proposed method to estimate the left-to-right shunt ratio was useful in determining the indication for fistula closure in a patient with HF and a significant shunt fistula. < Learning objective: A significant extracardiac left-to-right shunt more than 30–35% could cause heart failure with left ventricular dilatation similar to dilated cardiomyopathy. One can decide fistula closure with the finding of left-to-right shunt ratio calculated using a transcatheter oximetry run. It is mandatory that the venous oxygen saturation at the upper stream of fistula is determined precisely without the contamination of arterial blood. In this case, the oxygen saturation at the left anonymous vein substituted for it.> [ABSTRACT FROM AUTHOR]

Infantile hemangiomatosis is among the most common vascular tumours of childhood that is generally accepted as benign. Some cases may have multiple hemangiomas with organ involvement, especially of the liver. This case report will present the clinical and laboratory findings obtained during the treatment and follow-up of a 36-day-old female baby with hemangiomatosis with diffuse liver involvement, high-output heart failure, and pulmonary hypertension.

Patients with hepatic arteriovenous malformations rarely present with pulmonary hypertension. We report the case of a 3-month-old boy who developed severe pulmonary hypertension due to a hepatic arteriovenous malformation. The use of pulmonary vasodilators to treat the patient's pulmonary hypertension worsened his high-output heart failure. This is the first case in which emergency hepatectomy rescued a patient with hepatic arteriovenous malformations who developed pulmonary hypertension.