Low-output Heart Failure Research Articles

Reversible acute heart failure induced by thyrotoxic cardiomyopathy: A case report.

Thyrotoxic cardiomyopathy is a rare but severe complication of thyrotoxicosis, leading to episodes of acute heart failure. This case report highlights a rare presentation of thyrotoxic cardiomyopathy with low-output heart failure, emphasizing the importance of early diagnosis and comprehensive management. The report aims to increase awareness among clinicians about the potential reversibility of this condition and the effective strategies for managing such complex cases. This patient presented with dyspnea and chest constriction, without any antecedent predisposing factors. Subsequently, the patient abruptly manifested symptoms indicative of acute heart failure during outpatient consultation. Electrocardiography revealed rapid atrial fibrillation with type A preexcitation syndrome, whereas cardiac ultrasonography demonstrated global cardiac enlargement with a diminished ejection fraction (EF). After a comprehensive evaluation, the patient was diagnosed with thyrotoxic cardiomyopathy, acute heart failure, and atrial fibrillation with preexcitation syndrome. Immediate interventions comprised diuretic administration, oxygen therapy, and antiarrhythmic agents, addressing acute heart failure concomitant with preexcitation syndrome. Following a fortnight of comprehensive therapeutic measures, the patient was discharged with a prescription for oral medications, notably methimazole. Following the intervention, the patient showed significant improvement with the resolution of heart failure symptoms and dyspnea, restoration of sinus rhythm, improved left ventricular ejection fraction (LVEF improved from 36% to 45%), and normalization of thyroid function. These outcomes underscore the efficacy of the intervention strategy and offer a hopeful prognosis for similar cases. Thyrotoxicosis may cause cardiomyopathy in patients with heart failure that manifests as dilated cardiac chambers. Clinicians should carefully screen patients for this reversible condition. Diagnosis requires a comprehensive assessment of various tests, and the therapeutic goal is to restore normal thyroid function.

P437 HEART AND RHEUMATOLOGICAL DISEASE: A PICTURE OF ACUTE HEART FAILURE

Abstract Systemic sclerosis is a connective tissue disease characterized by endothelial dysfunction, hyper reactivity of fibroblasts and immunity abnormality in both humoral and mediated cells. Clinically, in addition to the typical skin involvement, mainly the face and fingers, is frequent involvement of lungs, heart and kidneys. Cardiac involvement, in combination with lung involvement, is considered to be the most important determinant of the prognosis of these patients. Cardiac involvement occurs in 15– 35% of cases but in autopsy surveys the incidence reaches 80%. The case we present concerns a woman of 65 years, admitted in December at the Department of Cardiology of our AOU for an episode of low–output heart failure with epigastralgia, sweating, and breathlessness. The cardiological history was almost silent; instead, it presented a history of chronic thyroiditis and a recent infection with SARS COV 2. The objective examination presented hypokinesis of basal pulmonary fields and pitting edema. The blood tests showed an increase in myocardial necrosis, BNP, creatininemia and inflammatory indices (VES, PCR, beta 2 microglobulin, ferritin, fibrinogen), normocytic normochromic anemia, hypogammaglobulinemia, hyperuricemia and proteinuria and hematuria. The echocardiogram showed severe biventricular dysfunction and moderate–grade mitral insufficiency. A coronary examination was performed that showed epicardial coronary vessels free from significant injury. The cardiac magnetic resonance showed a widespread late enhancement subendocardial of the ventricular and atrial chambers with non–vascular distribution suggestive of pathology on an autoimmune basis. Upon closer examination, multiple small telangiectasias were observed in the face, slight hyperpigmentation of the chest and back, and swelling of the hands. The antibody panel showed positivity of ANA and anti Scl70. The patient was thus addressed to a multi–specialist management in which therefore cardiologist and rheumatologist compare and support the treatment of this pathology with the goal of reducing the high mortality and morbidity that characterizes systemic scleroderma with cardiac involvement.

Abstract 11476: The Clot Thickens: Massive Left Ventricular Thrombus After Sub-Acute Myocardial Infarction

Introduction: Left ventricular thrombus (LVT) following myocardial infarction (MI) can affect up to 19.2% of patients with anterior wall MI. The mechanism is thought to be due to stasis from LV regional wall akinesia, endothelial injury from prolonged ischemia, and hypercoagulability from acute coronary syndrome. In patients with LVT after MI, anticoagulation choice and duration is still a matter of debate. Case Report: A 51-year-old woman with diabetes and prior anterior wall MI with LVT presented with non-healing diabetic leg wounds. One year ago at the time of the MI, transthoracic echocardiogram (TTE) showed a 4.0 x 1.3 cm mural thrombus. She was discharged on prasugrel and apixaban. Apixaban was discontinued after five months, with follow-up TTE showing resolution of LVT, with 30% LV ejection fraction and evidence of LV remodeling. This hospitalization, while awaiting discharge, the patient developed sudden undifferentiated shock requiring norepinephrine and dobutamine. Repeat TTE revealed a 6.0 x 5.5 cm apical LVT filling more than 50% of the LV cavity, with unchanged LV ejection fraction. Heparin drip was started. Prior to evaluation by cardiothoracic surgery, patient became acutely unresponsive, had a cardiac arrest, and expired. Cause of death suspected to be due to cardioembolic events, worsened with mixed shock and low-output heart failure from LVT. Discussion: Management of LVT after MI remains unclear. Current guidelines indicate treatment with vitamin K antagonist (VKA) for at least 3 - 6 months, and consideration of prophylactic anticoagulation with VKA for patients with apical dyskinesis after MI. Retrospectively, this patient may have benefitted from a prolonged course of anticoagulation given the extent of LV remodeling five months after initial event despite resolution of LVT. Anticoagulation must be evaluated on a case-by-case basis weighing propensity of thrombotic events with risk of bleeding.

675 A rare case of tako-tsubo syndrome in a patient with hypertrophic cardiomyopathy

Abstract Aims We know that basal septal hypertrophy is a rare and unique anatomical finding associated with hypertrophic cardiomyopathy (HCM). Tako-Tsubo cardiomyopathy (TTC) is a transient left ventricular systolic dysfunction induced by high physical or emotional stress. Its occurrence with HCM is unusual. However, this presentation occurs more often with the classic asymmetrical septal hypertrophy compared with the apical variant. This case demonstrates that the coexistence of TTC with septal HCM in an elderly patient may lead to a severe haemodynamic instability picture. Methods and results A 81-year-old female presented to the emergency department (ED) complaining of dyspnoea and chest pain lasting for 1 day. She had hypertension and dyslipidemia associated with a familial history of sudden death. On physical exam, we found a severe hypotension (systolic blood pressure of 80 mmHg) associated with bilateral rales at chest auscultation. Cardiac auscultation revealed a harsh systolic murmur, best heard over the left sternal border. Heart rate was 60 b.p.m. in sinus rhythm. Labs were significant for HS-I troponin of 6.035 ng/L (NV: ≤ 12) and NT-proBNP of 7.640 pg/ml (NV: ≤1800). A 12-leads electrocardiogram (ECG) at admission revealed a STEMI-like ST segment elevation from V2 to V6 (Figure 1A). For this reason she was urgently taken to the cath-lab where she was found to have tortuous but normal coronary arteries. After coronary angiography, a trans-thoracic echocardiogram (TTE) revealed a pathological LV hypertrophy with a septal diastolic thickness of 19 mm, depressed LV ejection fraction (LVEF) due to a severe apical ballooning. At continuous wave (CW)-Doppler there was a dynamic obstruction across the LV outflow tract (LVOT), with a late peak velocity of 4.9 m/s and an estimated peak gradient of 98 mmHg. The gradient was increased by a systolic anterior motion (SAM) of anterior mitral leaflet causing a moderate mitral regurgitation (MR). All these findings were consistent with obstructive septal HCM associated with Takotsubo cardiomyopathy. After treatment with intravenous diuretics and metoprolol (5 + 5 mg i.v. bolus followed by oral dose of 100 mg daily), her clinical condition markedly improved. One week later, ECG demonstrated deeply inverted T waves on antero-lateral leads and QT prolongation (501 ms). Three weeks later, after a complete resolution of the LV apical dyskinesia, LVEF normalized. LVOT gradient decreased to 20 mmHg, with a dynamic increase to 70 mmHg during Valsalva manoeuvre. Conclusions It is well known that TTC may be complicated by a reversible LVOT obstruction by itself but the combination with obstructive HCM can lead to low cardiac output and acute heart failure. This combination has been found to be not common and the correct treatment of this unusual type of cardiogenic shock is still unclear. Careful initial evaluation and continuous monitoring must be warranted in such rare cases. Supportive care afterward with beta blockers, along with echocardiogram surveillance, are the mainstay of management. Cardiologists, intensivisits, and clinicians alike need to recognize and comprehend the pathophysiology behind this unique clinical manifestation so that they may adjust their management and treatment accordingly.

Vascular Cases of High Output Heart Failure Masquerading as Low Output Heart Failure

Vascular Cases of High Output Heart Failure Masquerading as Low Output Heart Failure

The perils of beta-blockade and the promise of venoarterial extracorporeal membrane oxygenation in managing low-output heart failure in thyroid storm: a case report

The perils of beta-blockade and the promise of venoarterial extracorporeal membrane oxygenation in managing low-output heart failure in thyroid storm: a case report

Malnutrition Affects the Outcomes of Patients with Low-Output Heart Failure and Congestion.

This study aimed to investigate the relationship between malnutrition and outcomes in patients with decompensated severe systolic heart failure (HF) focusing on clinical presentations and medication use. This study prospectively enrolled 108 patients admitted for severe systolic HF with a left ventricular (LV) ejection fraction < 35%, low cardiac output, and high LV filling pressure. Five patients died during the index hospitalization, and the remaining 103 patients were followed up for 2 years. The primary endpoints were HF rehospitalization and all-cause mortality. Nutritional risk index (NRI) was calculated as (1.519 × serum albumin, g/L) + (41.7 × body weight/ideal body weight). Forty-four patients reached the study endpoints. An NRI ≤ 93 predicted events. The NRI ≤ 93 group had higher pulmonary artery systolic pressure, more edema over dependent parts, longer hospital stay, and more primary endpoints compared to the NRI > 93 group. The NRI ≤ 93 group received fewer evidence-based medications and more loop diuretics compared to the NRI > 93 group. NRI was an independent predictor of cardiovascular events [hazard ratio 0.902; 95% confidence interval (CI) 0.814-0.982 per 1 point increase; p = 0.012]. Low NRI was associated with a significantly higher use of loop diuretics [odds ratio (OR) 2.75; 95% CI 1.046-5.647; p = 0.004] and significantly lower use of beta blockers (OR 0.541; 95% CI 0.319-0.988; p = 0.002). Malnutrition assessed using the NRI was associated with cardiovascular events in the patients with severe systolic HF with low cardiac output and high LV filling pressure. Low NRI was associated with more diuretic and less beta blocker use.

Thyroid Dysfunction and Dysmetabolic Syndrome: The Need for Enhanced Thyrovigilance Strategies.

Thyroid dysfunction (TD) is common in metabolic disorders such as diabetes mellitus (DM), cardiovascular disease (CVD), obesity, dyslipidemia, hyperuricemia, kidney and liver dysfunctions, and polycystic ovary syndrome (PCOS). Subclinical hypothyroidism (SHypo) worsens glycemic control in patients with DM, and these patients, especially those with Type-1DM, have higher prevalence of TD. Both TD and DM increase CVD risk. Even minor alteration in thyroid hormone (TH) levels can alter cardiovascular function. While hyperthyroidism increases systolic blood pressure and leads to high-output heart failure, hypothyroidism increases diastolic blood pressure and leads to low-output heart failure. Chronic subclinical hyperthyroidism (SHyper) and SHypo both increase the risk of hypertension, coronary artery disease (CAD) events, CAD deaths, and total deaths. SHyper alters cardiac morphology and function. SHypo causes dyslipidemia and endothelial dysfunction and increases the risk for weight gain and obesity. Overweight and obese patients often have hyperleptinemia, which increases the secretion of thyroid stimulating hormone (TSH) and induces TD. Dyslipidemia associated with TD can increase serum uric acid levels. Hyperuricemia promotes inflammation and may increase the risk for dyslipidemia, atherosclerosis, and CVD. TD increases the risk for developing chronic kidney disease. In nephrotic syndrome, proteinuria is associated with urinary loss of TH leading to TD. Some correlation between TD and severity of liver disease is also seen. TD and PCOS have common risk factors and pathophysiological abnormalities. Hypothyroidism must be excluded before diagnosing PCOS. Current guidelines do not strongly recommend thyroid screening in the presence of all metabolic disorders. However, pragmatic thyrovigilance is required. Clinicians must stay alert to signs and symptoms of TD, maintain high clinical suspicion, and investigate thoroughly. Drug-induced TD should be considered when TH levels do not match clinical findings or when patients are on medications that can alter thyroid function.

Delayed diagnosis of dilated thyrotoxic cardiomyopathy with coexistent multifocal atrial tachycardia: a case report

BackgroundThyroid storm (TS) is a rare but potentially life-threatening sequelae of untreated or undertreated hyperthyroidism. While TS frequently causes high-output heart failure, low-output heart failure related to dilated cardiomyopathy (DCM) is extremely rare. Tachycardia is a common clinical presentation of TS, and β1-selective blockers are the first-line agents for treating TS-associated tachycardia. However, given that β-blockers have negative chronotropic and negative inotropic effects, amiodarone may be safe and effective for the treatment of TS-induced tachyarrhythmia in patients with moderate to severe heart failure. While long-term amiodarone administration causes hypothyroidism, or less frequently, hyperthyroidism, little is known about the effects of short-term amiodarone administration on thyroid function.Case presentationA 31-year-old healthy woman presented with worsening dyspnoea. She was tachycardic with multifocal atrial tachycardia (MAT) of 184 beats/min, confirmed by electrocardiogram. Echocardiographic findings were consistent with DCM, with an ejection fraction of 20%. Thus, she was initially diagnosed with acute heart failure due to DCM with coexistent MAT. Tachycardia persisted despite cardioversion attempts and treatment with multiple anti-arrhythmic drugs. Consequently, she rapidly progressed to cardiogenic shock and respiratory decompensation, which required intubation and an intra-aortic balloon pump support. Moreover, the undiagnosed Graves' disease, lack of suspicion, and postponed analysis of thyroid function tests led to a delayed diagnosis of TS. Amiodarone, which was initiated for MAT, unexpectedly ameliorated thyrotoxicosis, resulting in a euthyroid state and the patient’s significantly improved condition and cardiac function. She was discharged on day 40. Finally, she underwent total thyroidectomy; thyroid pathology was consisting with Graves' disease. Her postoperative course was uneventful.ConclusionsHerein, we describe a case of delayed diagnosis of dilated thyrotoxic cardiomyopathy with coexistent MAT. The patient required intensive care due to the catastrophic sequelae and was successfully treated with amiodarone. This is the first case report of TS-associated MAT and highlights the clinical importance of high suspicion of TS in de novo heart failure with any tachyarrhythmia or DCM of unknown etiology and the potential effects of short-term amiodarone administration in the treatment of TS.

MEDICATION INTERACTIONS CAUSING INSIDIOUS DIGOXIN TOXICITY IN AN ADVANCED HEART FAILURE PATIENT

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Although digoxin use has declined, its per patient toxicity incidence perhaps has not. Digoxin toxicity should be considered early in the patient presenting with gastrointestinal symptoms as they are at risk for renal dysfunction that may worsen cardiac function. CASE PRESENTATION: A 77-year-old male with a history of diabetes mellitus, atrial fibrillation, coronary artery disease, and ischemic cardiomyopathy presented with nausea, vomiting, diarrhea, and generalized fatigue worsening for one month. Presenting vitals: BP 80/60 mmHg, HR 60 bpm, temp. 34.2 C and pulse ox 99%. The patient was fully alert and oriented. Physical exam was largely unremarkable with clear lung exam, non-tender abdomen, no peripheral edema, and cardiac exam showing regular rhythm at 60 bpm. Labs showed K of 6 mmol/L, BUN of 79 mg/dL, Cr of 4.40 mg/dL, LA of 8.0 mmol/L, BNP 42000 pg/mL, and a normal CBC. Medication review significant for digoxin, amiodarone, and metformin use. Subsequently, digoxin level was found to be 6.0mcg/L and EKG showed ventricular paced rhythm. Given digoxin toxicity with hyperkalemia, digibind was administered. Patient was also found to have refractory metabolic acidosis in the setting of metformin toxicity, and so emergent sustained low efficiency dialysis was initiated. Right heart catheterization demonstrated low output heart failure, cardiac index 1.8L/min on dobutamine and norepinephrine. This low output was likely related to his renal failure and medication toxicities. The patient was sustained on inotropic agents and his pacemaker rate was increased. The patient had an aortic balloon pump placed while he and his family considered LVAD. Ultimately, the patient sustained further clinical deterioration at which time he and his family chose to pursue comfort measures. DISCUSSION: Advance heart failure is a challenging insidious disease. This is compounded by the fact that its treatments carry significant toxicities. In our case, the patient had recently reinitiated his prior amiodarone prescription. Both the prior medication discontinuation and subsequent re-initiation were unknown to his medical providers. The increase in digoxin levels when administered with amiodarone has long been observed and described. Digoxin toxicity presents with gastrointestinal symptoms as seen in our patient. Prolonged poor intake placed him at risk for renal dysfunction and perhaps subsequent worsening of his cardiac function due to the bidirectional relationship of cardiorenal syndrome. Frequent monitoring of digoxin levels is necessary in this patient population. Medication toxicities, interactions, and reconciliation are critical pieces of information in the critically ill patient. CONCLUSIONS: Drug interactions, such as the increase in serum digoxin when co-administered with amiodarone, can lead to the worsening of renal function which in the advanced heart failure patient, portends a poor prognosis. Reference #1: Haynes K, Heitjan D, Kanetsky P, Hennessy S. Declining public health burden of digoxin toxicity from 1991 to 2004. Clin Pharmacol Ther 2008;84:90-4. 10.1038/sj.clpt.6100458 Reference #2: Koonlawee Nademanee, et al. Amiodarone-digoxin interaction: Clinical significance, time course of development, potential pharmacokinetic mechanisms and therapeutic implications, Journal of the American College of Cardiology, Volume 4, Issue 1, 1984, Pages 111-116, ISSN 0735-1097. Reference #3: Forman DE, Butler J, Wang Y, Abraham WT, O’Connor CM, Gottlieb SS, Loh E, Massie BM, Rich MW, Stevenson LW, Young JB, Krumholz HM: Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure. J Am Coll Cardiol 43: 61–67, 2004 DISCLOSURES: No relevant relationships by Dustin Slagle, source=Web Response

Predictors of Successful Response to Afterload Reduction In Low-output Heart Failure with Reduced Ejection Fraction

Introduction Intravenous vasodilators such as sodium nitroprusside (SNP) are often used to reduce afterload in patients with acutely decompensated systolic heart failure and low cardiac output. However, there is a paucity of evidence guiding patient selection. The ability to identify patients that are most likely to respond with an improvement in cardiac output following the administration of SNP may help guide initial pharmacotherapy in the treatment of cardiogenic shock. Methods A retrospective review of patients admitted to our institution for pulmonary artery catheter (PAC) guided hemodynamic optimization of low-output HFrEF from 2018-2020 was performed. SNP response was defined as a CI > 2.2 L/min/m2 within 24 hours of initiation without the need for inotropes or mechanical circulatory support. Demographic, hemodynamic, and disease-specific variables prior to SNP initiation were compared between the two groups. The primary objective was to identify variables that predict response to SNP. Variables from the analysis were used to create a model to be utilized as a prediction assessment tool for response to SNP. Secondary endpoints compared survival, LVAD implantation, and transplantation between responders and non-responders. Results 77 patients were included for analysis, with 48 (62%) having successful response to SNP. Overall, patients with EF >20%, MAP > 80 mmHg, LVEDD 1.5 L/min/m2 on admit, and HR Conclusion We identified 5 demographic, hemodynamic, and clinical variables that were associated with a favorable response to afterload reduction in patients admitted with low-output heart failure. We created a SNP response prediction assessment model in order to help guide medication therapy for patients admitted with low-output heart failure. While our model did not predict survival or need for LVAD and transplantation in responders compared to failures with SNP therapy, utilization of this model in this patient population warrants further evaluation.

Digoxin Use in Cardiac Amyloidosis

Despite limited options for rate control of atrial fibrillation and for low-output heart failure seen in cardiac amyloidosis (CA), digoxin use is discouraged due to a reported increased risk of sensitivity and toxicity. We present our experience with digoxin use in patients with CA and report the event rate of suspected digoxin-related arrhythmias and toxicity. This is a retrospective study of patients with CA seen at our institution between November 1995 and October 2018. Patients were screened for a history of ≥7 days of continuous digoxin use and stratified based on amyloid precursor protein-transthyretin (ATTR) and immunoglobulin light chain (AL). Medical records were used to identify suspected digoxin-related arrhythmias and toxicity events. Digoxin was used in 69 patients (42 ATTR, 27 AL) for a median duration of 6 months (IQR, 1 to 16). Indication for use was rate control in 64% of patients and symptomatic heart failure management in 36%. Suspected digoxin-related arrhythmias and toxicity events occurred in 12% of patients. No deaths were attributed to digoxin use or toxicity, but 11 patients died while on digoxin-most due to progressive heart failure in the setting of CA. In conclusion, digoxin may be a therapeutic option for rate and symptom control for some patients with AL-CA and ATTR-CA. Rigorous patient selection is recommended, and patients should be closely monitored during digoxin administration.

Evaluation of cardiac dysfunction in adult zebrafish using high frequency echocardiography

AimsRecently, the zebrafish has gained attention as an innovative experimental model to decipher molecular and cellular mechanisms involved in cardiovascular development and diseases. Nevertheless, the use of zebrafish models has been challenged because the transparency of these fish, which allows for accurate cardiac evaluation, disappears in adulthood. In this study, the epicardial outline method was performed to investigate the feasibility of echocardiography in assessing cardiac function in pathological adult zebrafish. Materials and methodsWe attempted to estimate heart failure in adult zebrafish treated with three distinct regulators of cardiac function: phenylhydrazine hydrochloride (PHZ), doxorubicin (DOX), and ethanol. B-mode and Doppler images were evaluated at frequencies of up to 50 MHz and 40 MHz, respectively. The correlation between alterations in cardiac function, haemoglobin concentration, and myocardial histopathology were assessed. Key findingsCardiac output (CO) in PHZ-treated zebrafish was significantly higher than that in control zebrafish (151 ± 67 vs. 84 ± 37 μl/min, P = 0.004), whereas ejection fraction (EF) was lower (36.3 ± 10.9 vs. 50.9 ± 8.7%, P < 0.001), indicating typical high output heart failure derived from anaemia. Additionally, ventricular dysfunction in DOX-treated zebrafish was characterised by low CO (57 ± 38 μl/min) and EF (28.8 ± 10.4%), accompanied by an enlarged ventricle in diastole and systole, representing low output heart failure. For ethanol-treated zebrafish, EF was markedly reduced (39.6 ± 7.2%) indicating a dilated heart, while CO remained unchanged (90 ± 40 μl/min). SignificanceThe epicardial outline method is an effective way of using echocardiography to assess cardiac dysfunction in pathological adult zebrafish, unlocking a major bottleneck in this research field with limited cardiac functional assays.

TIME TO STRIP THE HEART? OPPORTUNE TIMING OF PERICARDIECTOMY IN TREATMENT OF IDIOPATHIC CONSTRICTIVE PERICARDITIS

Idiopathic constrictive pericarditis is a chronic inflammatory process ultimately leading to low cardiac output and advanced heart failure if untreated. The only definitive treatment is complete pericardiectomy; a long, technically complex and dangerous procedure. Timing of surgery is important as

Digoxin Use in Cardiac Amyloidosis

Introduction With limited options for rate control of atrial fibrillation in the setting of low-output heart failure (HF), digoxin may appear to be a reasonable option for patients with cardiac amyloidosis (CA). However, current guidelines, based on historical case reports and an in vitro study, state that digoxin should generally be avoided in CA due to increased sensitivity for digoxin toxicity. A recent study of 107 patients with AL amyloidosis given digoxin showed relative safety with cautious use, with 11% of patients developing significant arrhythmias. We describe our institution's experience with digoxin in patients with CA and the suspected digoxin-related arrhythmias and toxicity. Methods This is a retrospective examination of patients diagnosed with CA seen between November 1995 and October 2018 at the Cleveland Clinic. CA patients were screened for a history of digoxin use; patients with less than 7 days of digoxin use were excluded, as well as those with incomplete medical records. Suspected digoxin-related arrhythmias and toxicity events were defined as: unexplained altered mental status, use of digoxin immune fab, ventricular tachycardia/fibrillation, paroxysmal atrial tachycardia with 2:1 block, new-onset junctional rhythm, and symptomatic bradycardia. Results Of 756 patients with CA identified, 71 patients were treated with digoxin for ≥7 days: 42 with transthyretin (ATTR) CA and 29 with light chain (AL) CA. Median duration of digoxin therapy was 10 months (IQR 3-38) for the ATTR-CA cohort and 2 months (IQR 1-7) for the AL-CA cohort. Digoxin was used for rate control of atrial fibrillation in 66% of the total population (64% ATTR, 69% AL) and management of symptomatic HF in 34% (36% ATTR, 31% AL). Suspected digoxin-related arrhythmias and toxicity occurred in 10%, described in detail in Table 1. 21% of the digoxin population died while on therapy, but only one death may have been attributed to digoxin use or toxicity. Conclusions In carefully-selected patients with CA treated with digoxin, 90% did not have a digoxin-related adverse event over a median treatment duration of 10 months. 10% had an adverse event potentially attributable to digoxin, with one death that may or may not have been related. Despite current guidelines, digoxin may be used cautiously in selected patients with ATTR- or AL-CA who have no good options for rate control in atrial fibrillation or for low output heart failure. Risks and benefits of using digoxin in CA should be evaluated on a patient by patient basis.

An Approximation of Heart Failure Using Cardiovascular Simulation Toolbox

In this paper, we present the simulation of 5 different heart failures with the help of the Cardiovascular Simulation Toolbox (CVST) proposed by O. Barnea et al. at Tel-Aviv University. This is a modified version of the CVST, proposed by G.Ortiz; here, we show that the pathological failures can be covered by this tool. We varied the value of the tool blocks, included the results of the hemodynamic parameters and the P-V loop curves for each disease and compared them to the medical data to prove the effectiveness of the simulation. Based on these changes, we achieved an effective simulation of the following heart failures in the CVST: Diastolic Heart Failure (DHF), Systolic Heart Failure (SHF), Right Ventricle Heart Failure (RVHF), Low Output Heart Failure (LOHF) and High Output Heart Failure (HOHF).

Impact of Multivessel Coronary Artery Disease on Long Term Prognosis in Patients with ST-segment Elevation Myocardial Infarction

Abstract Background: A significant proportion of patients with ST-segment elevation myocardial infarction (STEMI) have multivessel coronary artery disease (MVD), and they are at high risk for recurrent cardiac events. The aim of the present study was to analyze the impact of MVD on long-term cardiovascular mortality in STEMI patients treated with primary percutaneous coronary intervention (pPCI). Method: This study included 3,115 consecutive STEMI patients hospitalized in the Coronary Care Unit of the Clinical Centre of Serbia, between November 2005 and January 2012. Patients were divided in two groups: MVD and no MVD. MVD disease was defined as stenosis greater than 50% by visual assessment in more than one major coronary artery. Primary PCI was limited to the infarct-related artery (IRA). Cardiovascular mortality was defined as any death from cardiovascular reason (myocardial reinfarction, low-output heart failure, and sudden death). Patients presenting with cardiogenic shock were excluded. Patients were followed-up for 6 years after enrollment. Results: Among 3,115 analyzed patients, 1,352 (43.4%) patients had no MVD and 1,763 (56.6%) had MVD; among patients with MVD, 926 (52.6%) had two-vessel disease and 837 (47.4%) had three-vessel disease. Compared with patients with single-vessel disease, patients with MVD were older, had longer pain duration, and presented more often with heart failure; they were more likely to have previous coronary artery disease, diabetes, hypertension, and chronic kidney disease; post-procedural flow TIMI &lt;3 was more frequently observed in patients with MVD than in patients with no MVD (5.9% vs. 3.1%, p &lt;0.001). Patients with MVD had lower left ventricular ejection fraction than patients with single-vessel disease: 45% (interquartile range [IQR] 40¬–55%) vs. 50% (IQR 43–55%), p &lt;0.001. Revascularization of non-IRA lesions was performed at index hospitalization in 1,075 (61%) patients, and in 602 (34.1%) patients revascularization was performed in the first few months after pPCI (median 1.5 months, IQR 1–2.5 months); coronary artery bypass grafting was performed in 291 (18.4%) patients and PCI (with stent implantation) in 1,368 (81.6%) patients. Six-year cardiovascular mortality was significantly higher in patients with MVD than in patients with single-vessel disease (10.4% vs. 4.6%, p &lt;0.001). In multivariate Cox regression analysis, MVD remained an independent predictor for 6-year cardiovascular mortality (HR 1.55, 95% CI 1.11–2.06, p = 0.041). Conclusion: In STEMI patients treated with pPCI, the presence of MVD remained an independent predictor for higher long-term cardiovascular mortality despite early revascularization of the remaining stenosis in non-IRA.

Hyperthyroidism-induced dilated cardiomyopathy

Hyperthyroidism is a common endocrine disorder with a prevalence of 1.3% in the generalpopulation, affecting more women than men. Prolonged hyperthyroidism without appropriatemanagement may lead to high output cardiac failure characterized by increases in heart rate,cardiac contractility, and cardiac output and by reductions in peripheral systemic vascularresistance. Dilated cardiomyopathy with impaired systolic function is rare and occurs in lessthan 1% of patients with thyrotoxicosis. The exact mechanism of hyperthyroidism-induceddilated cardiomyopathy is not well established. The combination of direct toxic effects of excessthyroid hormone along with prolonged tachycardia, arrhythmia, and a hyperdynamic state couldbe contributing factors. We present a case of a young woman with prolonged sinus tachycardiadue to a long history of medication non-compliance who developed dilated cardiomyopathywith low output heart failure. Early detection and management of hyperthyroidism are crucialto restore cardiac function.

Correlation between cardiovascular parameters and glaucomatous changes in the optic nerve in patients with low-output heart failure

Resumo Objetivos: Correlacionar parâmetros oftalmoscopicos e cardiovasculares em pacientes com diagnostico de insuficiencia cardiaca com fracao de ejecao reduzida (ICFER) e avaliar a associacao entre ICFER e alteracoes do nervo optico sugestivas de glaucoma. Metodos: Estudo descritivo, observacional, prospectivo, composto por amostra 30 pacientes com diagnostico de ICFER. Os pacientes foram submetidos ao exame oftalmologico, que incluiu biomicroscopia, avaliacao da acuidade visual, afericao da PIO (pressao intraocular), gonioscopia e medida de ECC (espessura central corneana). A avaliacao de parâmetros cardiovasculares, como PAM (pressao arterial media), FEVE (fracao de ejecao do ventriculo esquerdo), comorbidades e tempo de diagnostico de IC foi realizada a partir de revisao de prontuario medico. Arbitrariamente foi escolhido o olho esquerdo para analise estatistica dos dados. A correlacao estatistica foi realizada atraves do teste de Spearman, e a comparacao atraves do teste U de Mann-Whitney. Resultados: Observou-se uma alta prevalencia de atrofia peripapilar (73,3%), alem de uma correlacao positiva, moderada e estatisticamente significativa entre FEVE e PPO (pressao de perfusao ocular) (r = 0,517; p = 0,004). Apesar da ausencia de significância das comparacoes pelo Teste U de Mann-Whitney, evidenciou-se uma maior prevalencia de atrofia peripapilar nos pacientes que apresentavam uma menor PAM, menor FEVE e menor PPO. Conclusao: A ICFER pode ser um fator de risco para o desenvolvimento de alteracoes glaucomatosas no disco do nervo optico. A atrofia peripapilar e a baixa pressao de perfusao ocular resultantes do deficit contratil cardiaco podem estar relacionadas com a teoria vascular do desenvolvimento do glaucoma de pressao.

Low-output heart failure: A review of clinical status and meta-analysis of diagnosis and clinical management methods

Low-output heart failure: A review of clinical status and meta-analysis of diagnosis and clinical management methods