Acute High-Output Heart Failure with Pulmonary Hypertension and Severe Liver Injury Caused by Amlodipine Poisoning: A Case Report.

Acute high-output heart failure (HOHF) with pulmonary hypertension and liver injury caused by amlodipine poisoning is very rare. We report a 52-year-old woman who suffered from severe shock after an overdose of amlodipine. Hemodynamic monitoring showed that while her left ventricular systolic function and cardiac output were elevated, her systemic vascular resistance decreased significantly. At the same time, the size of her right heart, her central venous pressure, and the oxygen saturation of her central venous circulation all increased abnormally. The patient's circulatory function and right ventricular dysfunction gradually improved after large doses of vasopressors and detoxification measures. However, her bilirubin and transaminase levels increased significantly on hospital day 6, with a CT scan showing patchy, low-density areas in her liver along with ascites. After liver protective treatment and plasma exchange, the patient's liver function gradually recovered. A CT scan 4 months later showed all her liver abnormalities, including ascites, had resolved. The common etiologies of HOHF were excluded in this case, and significantly reduced systemic vascular resistance caused by amlodipine overdose was thought to be the primary pathophysiological basis of HOHF. The significant increase in venous return and pulmonary blood flow is considered to be the main mechanism of right ventricular dysfunction and pulmonary hypertension. Hypoxic hepatitis caused by a combination of hepatic congestion and distributive shock may be the most important factors causing liver injury in this patient. Whether amlodipine has other mechanisms leading to HOHF and pulmonary hypertension needs to be further studied. Considering the significant increase of right heart preload, aggressive fluid resuscitation should be done very cautiously in patients with HOHF and shock secondary to amlodipine overdose.

A Systematic Review Exploring the Impact of Arteriovenous Fistula Ligature on High-Output Heart Failure in Renal Transplant Recipients.

BACKGROUND: Cardiovascular disease is the most common cause of death in renal transplant recipients (RTrs). High-output heart failure (HoHF) is a classic problem of RTrs with patent arteriovenous fistulae (AVF). Central to the entire discipline of transplant nephrology is the ligation of AVF in RTrs, with a patent AVF presenting with signs and symptoms of HoHF. AVF ligation has long been a topic of great interest in this population. To date, little attention has been paid to the effects of arteriovenous graft ligation on HoHF. This study systematically reviews the data for AVF ligation, aiming to provide its impact on HoHF in RTrs. METHODS: The present study adopts the Preferred Reporting Items for Systematic Reviews and Meta-analysis 2020 guidelines. Published studies were identified using a search strategy in PubMed, Scopus, PubMed Central, Science Direct, and Medline. The primary inclusion criterion for this review was RTrs with a patent AVF who exhibited clinical or imaging findings of HoHF. Articles dating back to the last decade that involved the human species were included in our review, and the search was restricted to the English language. Studies involving both male and female genders and those describing the adult population (aged > 19 years) were also a part of our inclusion criteria. RESULTS: After applying eligibility criteria, our electronic search yielded 1,461 articles. A total of 16 studies that involved 18,735 subjects were included in our review, which comprised 6 cohort studies, 4 case reports, 2 randomized control trials, 2 narrative reviews, 1 meta-analysis, and 1 case series. While the risk of bias of the narrative reviews was low, 1 of the randomized control trials had some overall concerns. The meta-analysis included in our review had moderate risk of bias, while 4 of the 6 cohort studies were of good quality. All of the case reports and series included in our review were of good quality. Of the 12 studies that reported genders, 10,949 were male and 6,416 were female. There was a notable reduction in left ventricular mass, left ventricular mass index, left ventricular end diastolic dimension, cardiac output, velocity index, and systemic vascular resistance index upon AVF ligation. CONCLUSIONS: A complete resolution of the clinical signs and symptoms of HoHF can be anticipated after AVF ligation in RTrs. Clinicians should always be on the lookout for signs and symptoms of cardiovascular decompensation in asymptomatic RTrs.

32-year-old Traumatic Arteriovenous Fistula Presenting With Leg Ulcer and High-output Heart Failure.

Traumatic arteriovenous fistula (AVF) is not a common disorder, and dermatological signs and heart failure caused by AVF are rarely reported. We present the case of a 55-year-old woman who was referred for congestive heart failure symptoms. Echocardiography revealed preserved left ventricular ejection fraction. Due to edema of the right leg with a long-standing leg ulcer and palpable femoral thrill, duplex ultrasonography was performed. It showed an AVF between the right superficial femoral artery (SFA) and the right femoral vein (FV). The patient recalled a 32-year-old gunshot injury that was not medically treated. After the diagnosis of AVF she was referred to a surgeon for an AVF ligation, with subsequent resolution of her symptoms. The differential diagnosis of leg ulcer with leg edema should include the possibility of AVF as a cause.

Insuficiencia cardíaca de alto gasto asociada a fístula arteriovenosa: caso clínico / High output heart failure associated with arteriovenous fistula: clinical case / Insuficiência cardíaca de alto débito associada a fístula arteriovenosa: caso clínico

La creación de una fístula arteriovenosa (FAV) determina un incremento del gasto cardíaco, cuya magnitud está relacionada con el tamaño del cortocircuito. En el escenario adecuado esta puede conducir al desarrollo de insuficiencia cardíaca (IC) con alto gasto cardiaco. Se presenta el caso de un paciente que desarrolla IC luego de la confección de una FAV para hemodiálisis crónica y sus implicancias clínicas posteriores. Se revisan aspectos diagnósticos y terapéuticos referidos a la IC de alto gasto.

The creation of an arteriovenous fistula (AVF) determines an increase in cardiac output, the magnitude of which is related to the size of the shunt. In the right scenario, this can lead to the development of heart failure (HF) with high cardiac output. The case of a patient who develops HF after creating an AVF for chronic hemodialysis and its subsequent clinical implications is presented. Diagnostic and therapeutic aspects related to high-output HF are reviewed.

A criação de uma fístula arteriovenosa (FAV) determina aumento do débito cardíaco, cuja magnitude está relacionada ao tamanho do shunt. No cenário certo, isso pode levar ao desenvolvimento de insuficiência cardíaca (IC) com alto débito cardíaco. É apresentado o caso de um paciente que desenvolve IC após confecção de FAV para hemodiálise crônica e suas subsequentes implicações clínicas. Aspectos diagnósticos e terapêuticos relacionados à IC de alto débito são revisados.

Transition from Intravenous Epoprostenol to Treprostinil Due to Intolerable Side Effects in Patients With Pulmonary Arterial Hypertension.

Intravenous epoprostenol improves exercise capacity and survival in patients with pulmonary arterial hypertension (PAH); however, it has side effects. Reviewing the side effects associated with epoprostenol and treprostinil is essential for improving the long-term treatment strategies for PAH. This retrospective review included patients with PAH who transitioned from intravenous epoprostenol to intravenous treprostinil owing to intolerable side effects, including high cardiac output symptoms, ascites, and thrombocytopenia. Of the 85 patients who received epoprostenol at our hospital between 2013 and 2021, 16 (11 women), with a median age of 33 (range 26 to 40) years (including 12 with idiopathic PAH, 3 with hereditary PAH, and 1 with connective tissue disease pulmonary hypertension), had to switch from intravenous epoprostenol to treprostinil owing to the side effects. After transitioning, epoprostenol-associated intolerable side effects, such as high cardiac output symptoms, ascites, and thrombocytopenia, were ameliorated. In conclusion, for patients with PAH who have intolerable side effects from epoprostenol and have difficulty in continuing treatment, switching from epoprostenol to treprostinil may be an option. Switching treatment leads to better adherence and improved long-term prostacyclin therapy.

High cardiac output state due to pelvic arterio-venous shunt: a case report and review of the literature.

We are presenting a 35-year-old woman with past medical history of disseminated leiomyomatosis who presented with heart failure symptoms and was found to have post-capillary pulmonary hypertension and high cardiac output state in right heart catheterization secondary to a huge pelvic arterio-venous fistula.

Association between high cardiac output at altitude and acute mountain sickness: preliminary study on Mt. Fuji.

BACKGROUND: Acute mountain sickness (AMS) affects around 30% of people climbing Mt. Fuji, but its pathogenesis is incompletely understood. The influence of a rapid ascent to high altitude by climbing and summiting Mt. Fuji on cardiac function in the general population is unknown, and its association with altitude sickness has not been clarified. METHODS: Subjects climbing Mt. Fuji were included. Heart rate, oxygen saturation, systolic blood pressure, cardiac index (CI) and stroke volume index were measured multiple times at 120 m as baseline values and at Mt. Fuji Research Station (MFRS) at 3,775 m. Each value and its difference from the baseline value (Δ) of subjects with AMS (defined as Lake Louise Score [LLS] ≥ 3 with headache after sleeping at 3,775 m) were compared with those of non-AMS subjects. RESULTS: Eleven volunteers who climbed from 2,380 m to MFRS within 8 h and stayed overnight at MFRS were included. Four suffered AMS. Compared with the non-AMS subjects, CI in the AMS subjects was significantly higher than that before sleeping (median [interquartile range]: 4.9 [4.5, 5.0] vs. 3.8 [3.4, 3.9] mL/min/m2; p = 0.04), and their ΔCI was significantly higher before sleeping (1.6 [1.4, 2.1] vs. 0.2 [0.0, 0.7] mL/min/m2; p < 0.01) and after sleeping (0.7 [0.3, 1.7] vs. -0.2 [-0.5, 0.0] mL/min/m2; p < 0.01). ΔCI in the AMS subjects dropped significantly after sleeping versus before sleeping (3.8 [3.6, 4.5] vs. 4.9 [4.5, 5.0] mL/min/m2; p = 0.04). CONCLUSIONS: Higher values of CI and ΔCI were observed at high altitude in the AMS subjects. A high cardiac output might be associated with the development of AMS.

Pulmonary hypertension due to high cardiac output.

Pulmonary hypertension (PH) is usually associated with a normal or decreased cardiac output (CO). Less commonly, PH can occur in the context of a hyperdynamic circulation, characterized by high CO (>8 L/min) and/or cardiac index ≥4 L/min/m2 in the setting of a decreased systemic vascular resistance. PH due to high CO can occur due to multiple conditions and in general remains understudied. In this review article we describe the pathophysiology, etiology, diagnosis, hemodynamic characteristics, and management of PH in the setting of high CO. It is important to recognize this distinct entity as PH tends to improve with treatment of the underlying etiology and PH specific therapies may worsen the hemodynamic state.

Scapular renal cell carcinoma metastasis as a cause of high-output heart failure: a case report.

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.

A Case of High-Output Heart Failure.

CASE PRESENTATION: A 55-year-old woman with a medical history of hereditary hemorrhagic telangiectasia (HHT) complicated by recurrent nosebleeds, severe blood loss anemia, hepatic arterial-venous malformation (AVM), pulmonary hypertension, and severe tricuspid regurgitation presented to the HHT specialty clinic with acute hypoxic respiratory failure (new 3-L O2 requirement), weight gain, and volume overload. She was directly admitted to the pulmonary hypertension unit of our hospital. She had two recent admissions for similar symptoms thought to be due to worsening pulmonary arterial hypertension. In prior admissions, she had undergone right heart catheterization demonstrating mild pulmonary hypertension (pulmonary arterial pressure, 29 mm Hg, cardiac output by Fick 5.76, and cardiac index 3.22, mildly elevated pulmonary vascular resistance to 5.5 woods units). She would undergo diuresis with symptomatic improvement; however, after discharge she would rapidly develop recurrent heart failure symptoms. She reported compliance with guideline-directed medications, diuretics, and dietary restrictions and was still suffering severe symptoms. Notably she had previously elevated liver enzymes concerning for cirrhosis and had begun a workup to evaluate for causes of cirrhosis; she had a history of mild alcohol use, negative hepatitis viral serology, and no known history of liver disease.

Circulatory trajectories after out-of-hospital cardiac arrest: a prospective cohort study.

BACKGROUND: Circulatory failure frequently occurs after out-of-hospital cardiac arrest (OHCA) and is part of post-cardiac arrest syndrome (PCAS). The aim of this study was to investigate circulatory disturbances in PCAS by assessing the circulatory trajectory during treatment in the intensive care unit (ICU). METHODS: This was a prospective single-center observational cohort study of patients after OHCA. Circulation was continuously and invasively monitored from the time of admission through the following five days. Every hour, patients were classified into one of three predefined circulatory states, yielding a longitudinal sequence of states for each patient. We used sequence analysis to describe the overall circulatory development and to identify clusters of patients with similar circulatory trajectories. We used ordered logistic regression to identify predictors for cluster membership. RESULTS: Among 71 patients admitted to the ICU after OHCA during the study period, 50 were included in the study. The overall circulatory development after OHCA was two-phased. Low cardiac output (CO) and high systemic vascular resistance (SVR) characterized the initial phase, whereas high CO and low SVR characterized the later phase. Most patients were stabilized with respect to circulatory state within 72 h after cardiac arrest. We identified four clusters of circulatory trajectories. Initial shockable cardiac rhythm was associated with a favorable circulatory trajectory, whereas low base excess at admission was associated with an unfavorable circulatory trajectory. CONCLUSION: Circulatory failure after OHCA exhibits time-dependent characteristics. We identified four distinct circulatory trajectories and their characteristics. These findings may guide clinical support for circulatory failure after OHCA. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02648061.

Translational Sciences in Cardiac Failure Secondary to Arteriovenous Fistula in Hemodialysis Patients.

High-output cardiac failure is a rare form of heart failure associated with the formation of arteriovenous fistula (AVF) in hemodialysis patients. The pathophysiology underlying the HOCF is complex and multifactorial. Presence of AVF can cause long term hemodynamic changes that ultimately lead to increased cardiac output and consequently cardiac failure. A number of risk factors have been associated with the development of HOCF post-AVF construction, including male sex, a proximally located AVF and a state of volume overload. Dysregulation of tissue inhibitor of matrix metalloproteinase 4, Sirtuin-1 and Sirtuin-3 gene expression have been associated with the development of heart failure. The differences observed between genders have been attributed to altered activity of the ß-adrenoceptor system. Numerous biomarkers including cardiac troponin T and I, atrial natriuretic peptide, brain natriuretic peptide among others have shown both prognostic and diagnostic potential; however further research is needed to establish their utility in clinical practice for patients with AVF associated HOCF. In recent years risk stratification models have been developed to help identify patients at the highest risk of developing HOCF post AVF which could be revolutionary in its identification and management. Potential options for managing HOCF post-AVF include AVF ligation, banding and anastoplasty however these procedures are not without their own associated risks. In this review, we discuss the pathophysiology, risk stratification and management of patients with AVF associated HOCF.

Systemic Artery Vasoconstrictor Therapy in Fontan Patients with High Cardiac Output-Heart Failure: A Single-Center Experience.

Failed Fontan Patients with high cardiac output (CO) heart failure (HF) might have vasodilatory syndrome and markedly high mortality rates. The aim of this study was to review the clinical effects of vasoconstrictor therapy (VCT) for failed Fontan hemodynamics. We retrospectively reviewed 10 consecutive patients with Fontan failure (median age, 33 years) and high CO-HF who had received VCT. The hemodynamics were characterized by high central venous pressure (CVP: median, 16 mm Hg), low systolic blood pressure (median, 83 mm Hg), low systemic vascular resistance (median, 8.8 U·m2), high cardiac index (median, 4.6 L/min/m2), and low arterial oxygen saturation (median, 89%). VCT included intravenous noradrenaline infusion for five unstable patients, oral midodrine administration for nine stable patients, and both for four patients. After VCT introduction with a median interval of 1.7 months, the median systolic blood pressure (102 mm Hg, p = 0.004), arterial oxygen saturation (90%, p = 0.03), and systemic vascular resistance (12.1 U·m2, p = 0.13) increased without significant changes in CVP or cardiac index. After a median follow-up of 21 months, the number of readmissions per year decreased from 4 (1-11) to 1 (0-9) (p = 0.25), and there were no VCT-related complications; however, five patients (50%) developed hepatic encephalopathy, and six patients (60%) eventually died. VCT was safely introduced and could prevent the rapidly deteriorating Fontan hemodynamics. VCT could be an effective therapeutic strategy for failed Fontan patients with high CO-HF.

Iatrogenic Arteriovenous Fistula Formation after Endovenous Laser Treatment Resulting in High-output Cardiac Failure: A Case Report and Review of the Literature.

Formation of a clinically significant iatrogenic arteriovenous fistula after endovenous laser treatment of the great saphenous vein is an extremely rare complication. Because of the infrequency of reported cases, there is no clear consensus on how to best manage this complication. We present a unique case of an iatrogenic high-output superficial femoral artery-common femoral vein fistula resulting in right heart failure and a distal deep vein thrombosis. Deployment of a covered arterial stent graft resulted in resolution of the arteriovenous fistula and high-output cardiac state. Clinically significant arteriovenous fistulas resulting from inadvertent vessel injury during endovenous laser treatment appear to be amenable to percutaneous endovascular interventions. During these challenging endovascular cases, intravascular ultrasonography can be used to help delineate the morphology of the fistula tract and obtain vessel measurements to ensure accurate endoprosthesis sizing and placement.

Arterio-Hepatic Venous Fistula Following Liver Biopsy: A Rare Case Report and Literature Review.

Arterio-hepatic venous fistula (AHVF) is an exceedingly rare phenomenon compared to arterio-portal venous fistula with only 8 cases reported in world literature. Many listed causes can be attributed to the development of there are no reported cases of AHVF following a core-needle biopsy. We report a case of 38 year-old-female with EHPVO, who underwent splenectomy with a proximal splenorenal shunt. She had an injury to left hepatic artery, consequent to a blind intra-operative core needle biopsy from the liver, which led to the development of a fistulous connection between left hepatic artery and middle hepatic vein causing high output cardiac failure. She was successfully managed with trans-arterial embolization. The present review emphasizes the possibility of AHVF following a liver biopsy and the role of digital subtraction angiography in the diagnosis, therapeutic intravascular interventions, and follow-up.

Subaortic Membranes in Patients With Hereditary Hemorrhagic Telangiectasia and Liver Vascular Malformations.

Background Patients with hereditary hemorrhagic telangiectasia have liver vascular malformations that can cause high-output cardiac failure (HOCF). Known sequelae include pulmonary hypertension, tricuspid regurgitation, and atrial fibrillation. Methods and Results The objectives of this study were to describe the clinical, echocardiographic, and hemodynamic characteristics and prognosis of hereditary hemorrhagic telangiectasia patients with HOCF who were found to have a subaortic membrane (SAoM). A retrospective observational analysis comparing patients with and without SAoM was performed. Among a cohort of patients with HOCF, 9 were found to have a SAoM in the left ventricular outflow tract by echocardiography (all female, mean age 64.8±4.0 years). The SAoM was discrete and located in the left ventricular outflow tract 1.1±0.1 cm below the aortic annular plane. It caused turbulent flow, mild obstruction (peak velocity 2.8±0.2 m/s, peak gradient 32±4 mm Hg), and no more than mild aortic insufficiency. Patients with SAoM (n=9) had higher cardiac output (12.1±1.3 versus 9.3±0.7 L/min, P=0.04) and mean pulmonary artery pressures (36±3 versus 28±2 mm Hg, P=0.03) compared with those without SAoM (n=19) during right heart catheterization. Genetic analysis revealed activin receptor-like kinase 1 mutations in each of the 8 patients with SAoM who had available test results. The presence of a SAoM was associated with a trend towards higher 5-year mortality during follow-up. Conclusions SAoM with mild obstruction occurs in patients with hereditary hemorrhagic telangiectasia and HOCF. SAoM was associated with features of more advanced HOCF and poor outcomes.