Project description:Iatrogenic complications may manifest in a variety of ways. We present the case of an 86-year-old woman who underwent a percutaneous coronary intervention with a drug-eluting stent for non-ST-segment elevation myocardial infarction followed by leadless pacemaker placement through a femoral approach. Her post-procedure course was complicated by new onset high-output heart failure secondary to iatrogenic arteriovenous fistula formation, requiring covered stent placement. (Level of Difficulty: Advanced.).
Project description:BackgroundPrimary 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 summaryA 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.DiscussionPrimary 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.
Project description:Fistulous communications between the common iliac arteries and inferior vena cava are very uncommon and usually occur as a result of trauma, aneurysmal rupture, or endovascular repair. They can present with signs of high output cardiac failure including hypotension, venous congestion, and pulmonary hypertension. This case outlines the utility of CTA in diagnosing iliocaval fistulas and the importance of considering this diagnosis in a patient with signs of right heart strain and high output cardiac failure.
Project description:BackgroundArteriovenous (AV) fistulas are considered the gold standard for ensuring safe and long-term vascular access in patients with haemodialysis-dependent end-stage renal disease. However, previous studies demonstrated that high-flow AV fistulas might add additional cardiovascular burden in the post-transplant setting, leading to frequent fistula closure in this population. Currently, there is no consensus regarding management of high-flow fistulas in post-transplant patients with stable kidney function. The present randomized controlled trial examines the effect of prophylactic AV fistula closure on high-output heart failure.MethodsTwenty-eight kidney transplant patients with stable graft function, absence of pre-existing severe cardiac failure, and brachial arterial flow rate of at least 1,500 mL/min were recruited and randomized in a 1:1 ratio to an intervention and control group, respectively. The intervention group was subject to immediate fistula ligature. Patients within the control group were referred to fistula ligature only if the main study endpoint high-output heart failure was reached. The latter was defined by the presence of at least 1 clinical sign (i.e., worsening NYHA score) and at least 2 of the following echocardiographic parameters: diameter of right atrium (major) >53 mm, right atrium (minor) >44 mm, inferior vena cava ≥21 mm, right pulmonary artery >20 mm, TAPSE <16 mm, systolic pulmonal artery pressure >40 mm Hg, and/or left ventricular eccentricity index <1. During a 24-month follow-up period, quarterly measurements of kidney function, NT-proBNP, and lactate dehydrogenase as well as a biannual echocardiographic check-up were performed.ResultsHigh-output heart failure attributable to high-flow fistula was reported in 5 of 13 control patients (38.5%), whereas no patient in the intervention group presented with clinical and echocardiographic signs of high-output heart failure during the follow-up period. Thus, prophylactic ligature of high-flow fistulas avoided high-output heart failure in our patient population (p = 0.013). Three patients in the control group, however, had to undergo fistula ligature due to aneurysm formation (n = 2) and steal phenomenon (n = 1). Median NT-proBNP levels decreased from 317 ng/L pre-ligature to 223 ng/L post-ligature (p = 0.003). Serum creatinine levels did not significantly differ before and after AV fistula ligature (1.69 vs. 1.60 mg/dL, respectively, p = 0.059). Improvement of echocardiographic findings (e.g., a decrease in systolic pulmonary arterial pressure) was found in 7 of 8 ligature patients but did not reach statistical significance.ConclusionProphylactic ligature of high-flow AV fistulas after kidney transplantation can avoid high-output heart failure, and a more liberal approach to close AV fistulas might be justified.
Project description:We present the case of a 63-year-old woman presenting with a huge pelvic and retroperitoneal high flow arteriovenous malformation (AVM) causing high-output heart failure, who was treated with combined therapies, including transarterial embolization with n-butyl cyanoacrylate-iodized oil mixture (NBCA-lip) and coils for the right ovarian, both internal iliac, 3rd and 4th lumber arteries, venous sclerotherapy using coils and ethanolamine oleate (EO) for the right ovarian and both internal iliac veins with balloon-occluded retrograde transvenous obliteration technique, and direct percutaneous sclerotherapy using the NBCA-lip and EO for the large nidus of AVM under outflow control using occlusion balloon catheters. <Learning objective: Huge arteriovenous fistulae or malformation (AVF/M) are potentially life threatening due to the potential for spontaneous hemorrhaging and high-output heart failure and are notoriously difficult to diagnose and treat. To improve the high-output heart failure, intensive and invasive combined treatments for huge AVF/M are needed including transarterial and transvenous embolization and sclerotherapy and percutaneous nidus sclerotherapy.>.
Project description:A man affected by hereditary hemorrhagic telangiectasia who had chronic severe hypoxemia is presented. This hypoxemia was synergistically caused by high-output heart failure due to severe hepatic shunts and multiple pulmonary arteriovenous shunts. The symptomatic combination is rare, and genetic testing showed a novel endoglin mutation. (Level of Difficulty: Advanced.).
Project description:BackgroundHigh-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 summaryA 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.DiscussionHigh-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.
Project description:In hemodialysis patients, a native arteriovenous fistula (AVF) is the preferred form of permanent vascular access. Despite recent improvements, vascular access dysfunction remains an important cause of morbidity in these patients. In this prospective observational cohort study, we evaluated potential risk factors for native AVF dysfunction. We included 68 patients with chronic renal disease stage 5 eligible for AVF construction at the Department of General and Vascular Surgery, Central Clinical Hospital Ministry of Internal Affairs, Warsaw, Poland. Patient characteristics and biochemical parameters associated with increased risk for AVF failure were identified using Cox proportional hazards models. Vessel biopsies were analyzed for inflammatory cells and potential associations with biochemical parameters. In multivariable analysis, independent predictors of AVF dysfunction were the number of white blood cells (hazard ratio [HR] 1.67; 95% confidence interval [CI] 1.24 to 2.25; p<0.001), monocyte number (HR 0.02; 95% CI 0.00 to 0.21; p = 0.001), and red blood cell distribution width (RDW) (HR 1.44; 95% CI 1.17 to 1.78; p<0.001). RDW was the only significant factor in receiver operating characteristic curve analysis (area under the curve 0.644; CI 0.51 to 0.76; p = 0.046). RDW>16.2% was associated with a significantly reduced AVF patency frequency 24 months after surgery. Immunohistochemical analysis revealed CD45-positive cells in the artery/vein of 39% of patients and CD68-positive cells in 37%. Patients with CD68-positive cells in the vessels had significantly higher white blood cell count. We conclude that RDW, a readily available laboratory value, is a novel prognostic marker for AVF failure. Further studies are warranted to establish the mechanistic link between high RDW and AVF failure.
Project description:A 56-year-old man who had twice previously undergone orthotopic heart transplantation was admitted with dyspnea and heart failure symptoms. A biopsy excluded rejection. Left heart catheterization revealed a coronary cameral fistula. After the patient was given mild diuretics, his condition improved. No significant fistula flow was detected, and he was discharged. Several months later, the patient was readmitted with worsening chest pain and dyspnea. Left ventricular end-diastolic pressure and flow through the fistula were increased. To correct the coronary cameral fistula, we performed a coil embolization without complications. Several months later at follow-up, the patient's symptoms had resolved, and his left ventricular end-diastolic pressure had normalized. We conclude that coronary fistulas may be caused by trauma to the heart during the de-airing process, which may be prevented in the future with the development of safer and more effective de-airing techniques.
Project description: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.Learning objectives•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.