scholarly journals Elevated Lactate Levels as a Predictor of Early Mortality in Patients with Severe LV Dysfunction without Shock or Hypoxemia

2019 ◽  
Vol 04 (02) ◽  
pp. 068-071
Author(s):  
Shravan Kumar Chetti ◽  
Sandeep Moode ◽  
Indrani Garre ◽  
Lalita Nemani

Abstract Background Hyperlactatemia in intensive coronary care unit (ICCU) admitted patients who are critically ill must be considered to be related to tissue hypoxia/hypoperfusion. The routine measurement of lactate levels and its significance is still unclear in ICCU patients with left ventricular ejection fraction (LVEF) < 35% without hypotension and/or hypoxia. Methods and Materials A prospective study was conducted for six months between January 2018 and June 2018 in our institute. Age ≥18 years who admitted to the ICCU with LVEF less than 35% were included. Results Total of 104 patients were included after met inclusion and exclusion criteria and consented to enrolment in the study. The most common age group involved was between 50 and 70 years (46.2% of the patients) with a mean age of 52.5 ± 16.3 years. Mean lactate levels in the study population were 1.9 mmol/L. Mortality was noted in five patients (4%) in whom there were mean lactate levels of 2.58 ± 0.37 mmol/L. In the present study population, the patients with elevated lactate levels had early mortality with a p-value of 0.005 (95% CI for difference = 0.604–1.596). The average duration of stay in ICCU in the study population was 3.3 ± 1.2 days, which was in correlation with elevated serum lactate levels. The mean pH of the study population was 7.2 ± 0.19, and mean pH in the mortality group was 7.06 ± 0.21, which was not statistically significant with those of the study population. Conclusions From our study, patients without signs of heart failure and cardiogenic shock had increased mortality when blood lactate level was over or equal to 2.5 mmol/L. So it may be used as an adjunct in identifying patients with a higher risk of mortality even without signs of heart failure, cardiogenic shock. In conclusion, according to our data, ICCU admitted patients with LVEF < 35%, blood lactate is a prognostic marker for early mortality.

2019 ◽  
Vol 46 (2) ◽  
pp. 124-127 ◽  
Author(s):  
Majed Afana ◽  
Rishi J. Panchal ◽  
Rebecca M. Simon ◽  
Amal Hejab ◽  
Sharon W. Lahiri ◽  
...  

Pheochromocytoma, a rare catecholamine-secreting tumor, typically manifests itself with paroxysmal hypertension, tachycardia, headache, and diaphoresis. Less often, symptoms related to substantial hemodynamic compromise and cardiogenic shock occur. We report the case of a 66-year-old woman who presented with abdominal pain. Examination revealed a large right adrenal mass, cardiogenic shock, and severe heart failure in the presence of normal coronary arteries. Within days, the patient's hemodynamic status and left ventricular ejection fraction improved markedly. Results of imaging and biochemical tests confirmed the diagnosis of pheochromocytoma-induced takotsubo cardiomyopathy. Medical therapy and right adrenalectomy resolved the patient's heart failure, and she was asymptomatic postoperatively. We recommend awareness of the link between pheochromocytoma and takotsubo cardiomyopathy, and we discuss relevant diagnostic and management principles.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jaydeep J. Raval ◽  
Christina Rodriguez Ruiz ◽  
James Heywood ◽  
Jason J. Weiner

Abstract Background Although systemic lupus erythematosus (SLE) can affect the cardiovascular system in many ways with diverse presentations, a severe cardiogenic shock secondary to SLE myocarditis is infrequently described in the medical literature. Variable presenting features of SLE myocarditis can also make the diagnosis challenging. This case report will allow learners to consider SLE myocarditis in the differential and appreciate the diagnostic uncertainty. Case presentation A 20-year-old Filipino male presented with acute dyspnea, pleuritic chest pain, fevers, and diffuse rash after being diagnosed with SLE six months ago and treated with hydroxychloroquine. Labs were notable for leukopenia, non-nephrotic range proteinuria, elevated cardiac biomarkers, inflammatory markers, low complements, and serologies suggestive of active SLE. Broad-spectrum IV antibiotics and corticosteroids were initiated for sepsis and SLE activity. Blood cultures were positive for MSSA with likely skin source. An electrocardiogram showed diffuse ST-segment elevations without ischemic changes. CT chest demonstrated bilateral pleural and pericardial effusions with dense consolidations. Transthoracic and transesophageal echocardiogram demonstrated reduced left ventricular ejection fraction (LVEF) 45% with no valvular pathology suggestive of endocarditis. Although MSSA bacteremia resolved, the patient rapidly developed cardiopulmonary decline with a repeat echocardiogram demonstrating LVEF < 10%. A Cardiac MRI was a nondiagnostic study to elucidate an etiology of decompensation given inability to perform late gadolinium enhancement. Later, cardiac catheterization revealed normal cardiac output with non-obstructive coronary artery disease. As there was no clear etiology explaining his dramatic heart failure, endomyocardial biopsy was obtained demonstrating diffuse myofiber degeneration and inflammation. These pathological findings, in addition to skin biopsy demonstrating lichenoid dermatitis with a granular “full house” pattern was most consistent with SLE myocarditis. Furthermore, aggressive SLE-directed therapy demonstrated near full recovery of his heart failure. Conclusion Although myocarditis during SLE flare is a well-described cardiac manifestation, progression to cardiogenic shock is infrequent and fatal. As such, SLE myocarditis should be promptly considered. Given the heterogenous presentation of SLE, combination of serologic evaluation, advanced imaging, and myocardial biopsies can be helpful when diagnostic uncertainty exists. Our case highlights diagnostic methods and clinical course of a de novo presentation of cardiogenic shock from SLE myocarditis, then rapid improvement.


Open Heart ◽  
2020 ◽  
Vol 7 (1) ◽  
pp. e001065
Author(s):  
Mia Bertic ◽  
Christopher B Fordyce ◽  
Nima Moghaddam ◽  
John Cairns ◽  
Martha Mackay ◽  
...  

BackgroundST-segment elevation myocardial infarction (STEMI) outcomes are influenced by the location of the culprit vessel with worse outcomes portended with a left anterior descending (LAD) culprit lesion. However, relatively little is known about the independent association of LAD involvement with clinical outcomes of patients with STEMI with and without out-of-hospital cardiac arrest (OHCA).MethodsWe identified 91 patients with and 929 without a preceding OHCA within the Vancouver Coastal Health Authority who presented with an acute STEMI and underwent primary percutaneous coronary intervention between 26 June 2007 and 31 March 2016.ResultsPatients with STEMI with OHCA had higher rates of in-hospital cardiac arrest (43.3% vs 8.3%, p<0.001), heart failure (50.5% vs 11.3%, p<0.001), cardiogenic shock (49.5% vs 5.7%, p<0.001), mortality (35.2% vs 3.3%, p<0.001) and reduced left ventricular ejection fraction (LVEF; 42.9% vs 47.3%, p<0.001) compared with those without OHCA. Among patients without OHCA, LAD involvement was associated with increased heart failure (18.1% vs 5.2%, p<0.001), in-hospital cardiac arrest (10.7% vs 6.2%, p<0.014), cardiogenic shock (8.4% vs 3.3%, p<0.001), reduced LVEF (43.0% vs 51.2%, p<0.001) and mortality (5.2% vs 1.3%, p=0.003) compared with patients without LAD involvement. With the exception of LVEF, these associations were not seen among patients with STEMI with OHCA and an LAD culprit. The presence of an LAD culprit was not independently associated with increased hospital mortality among patients with OHCA after adjusting for potential confounding factors.ConclusionOur study has demonstrated a differential impact of LAD involvement on clinical outcomes among patients with STEMI who present with and without OHCA. Our data highlight the complexity surrounding the prognostication following OHCA complicating STEMI and demonstrate that other mechanisms other than LAD involvement contribute to the high mortality associated with OHCA as a result of STEMI.


2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Alessandro Maloberti ◽  
Paola Rebora ◽  
Marco Centola ◽  
Nuccia Morici ◽  
Alice Sacco ◽  
...  

Abstract Aims we focused on the role of Uric Acid (UA) as a possible determinant of Heart Failure (HF) related issues in Acute Coronary Syndromes (ACS) patients. Main outcome were acute HF and cardiogenic shock at admission, secondary outcomes were the need of Non Invasive Ventilation (NIV) use and the admission Left Ventricular Ejection Fraction (LVEF). Methods and results we consecutively enrolled 1269 ACS patients admitted to the cardiological Intensive Care Unit of the Niguarda and San Paolo hospitals (Milan, Italy) from June 2016 to June 2019. Hyperuricaemia was defined as a value higher than 6 mg/dl for females and 7 mg/dl for males. All the evaluated outcomes occurred more frequently in the hyperuricemic subjects (n = 292): acute HF 35.8 vs. 11.1% (P &lt; 0.0001), cardiogenic shock 10 vs. 3.1% (P &lt; 0.0001), NIV 24.1 vs. 5.1% (P &lt; 0.0001) with lower admission LVEF (42.9 ± 12.8 vs. 49.6 ± 9.9, P &lt; 0.0001). By multivariable analyses, UA was confirmed to be significantly associated with all the outcomes with the following odds ratio (OR): acute HF OR = 1.119; 95% CI: 1.019–1.229; cardiogenic shock OR = 1.157; 95% CI: 1.001–1.337; NIV use OR = 1.208; 95% CI: 1.078–1.354; LVEF β = −0.999; 95% CI: −1.413 to − 0.586. Conclusions The main result of our study was the finding of a significant association between UA and acute HF, cardiogenic shock, NIV use and LVEF. Due to the cross-sectional nature of our study no definite answer on the direction of these relationship can be drawn and further longitudinal study on UA changes over time during an ACS hospitalization are needed.


2020 ◽  
Vol 90 (1-2) ◽  
pp. 49-58 ◽  
Author(s):  
Wang Chunbin ◽  
Wang Han ◽  
Cai Lin

Abstract. Vitamin D deficiency commonly occurs in chronic heart failure. Whether additional vitamin D supplementation can be beneficial to adults with chronic heart failure remains unclear. We conducted a meta-analysis to derive a more precise estimation. PubMed, Embase, and Cochrane databases were searched on September 8, 2016. Seven randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in adults with chronic heart failure, and comprised 592 patients, were included in the analysis. Compared to placebo, vitamin D, at doses ranging from 2,000 IU/day to 50,000 IU/week, could not improve left ventricular ejection fraction (Weighted mean difference, WMD = 3.31, 95% confidence interval, CL = −0.93 to 7.55, P < 0.001, I2 = 92.1%); it also exerts no beneficial effects on the 6 minute walk distance (WMD = 18.84, 95% CL = −24.85 to 62.52, P = 0.276, I2 = 22.4%) and natriuretic peptide (Standardized mean difference, SMD = −0.39, 95% confidence interval CL = −0.48 to 0.69, P < 0.001, I2 = 92.4%). However, a dose-response analysis from two studies demonstrated an improved left ventricular ejection fraction with vitamin D at a dose of 4,000 IU/day (WMD = 6.58, 95% confidence interval CL = −4.04 to 9.13, P = 0.134, I2 = 55.4%). The results showed that high dose vitamin D treatment could potentially benefit adults with chronic heart failure, but more randomized controlled trials are required to confirm this result.


2011 ◽  
Vol 7 (1) ◽  
pp. 29
Author(s):  
Charlotte Eitel ◽  
Gerhard Hindricks ◽  
Christopher Piorkowski ◽  
◽  
◽  
...  

Cardiac resynchronisation therapy (CRT) is an efficacious and cost-effective therapy in patients with highly symptomatic systolic heart failure and delayed ventricular conduction. Current guidelines recommend CRT as a class I indication for patients with sinus rhythm, New York Heart Association (NYHA) functional class III or ambulatory class IV, a QRS duration ≥120ms, and left ventricular ejection fraction (LVEF) ≤35%, despite optimal pharmacological therapy. Recent trials resulted in an extension of current recommendations to patients with mild heart failure, patients with atrial fibrillation, and patients with an indication for permanent right ventricular pacing with the aim of morbidity reduction. The effectiveness of CRT in patients with narrow QRS, patients with end-stage heart failure and cardiogenic shock, and patients with an LVEF >35% still needs to be proved. This article reviews current evidence and clinical applications of CRT in heart failure and provides an outlook on future developments.


2012 ◽  
Vol 9 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Otto A Smiseth ◽  
Anders Opdahl ◽  
Espen Boe ◽  
Helge Skulstad

Heart failure with preserved left ventricular ejection fraction (HF-PEF), sometimes named diastolic heart failure, is a common condition most frequently seen in the elderly and is associated with arterial hypertension and left ventricular (LV) hypertrophy. Symptoms are attributed to a stiff left ventricle with compensatory elevation of filling pressure and reduced ability to increase stroke volume by the Frank-Starling mechanism. LV interaction with stiff arteries aggravates these problems. Prognosis is almost as severe as for heart failure with reduced ejection fraction (HF-REF), in part reflecting co-morbidities. Before the diagnosis of HF-PEF is made, non-cardiac etiologies must be excluded. Due to the non-specific nature of heart failure symptoms, it is essential to search for objective evidence of diastolic dysfunction which, in the absence of invasive data, is done by echocardiography and demonstration of signs of elevated LV filling pressure, impaired LV relaxation, or increased LV diastolic stiffness. Antihypertensive treatment can effectively prevent HF-PEF. Treatment of HF-PEF is symptomatic, with similar drugs as in HF-REF.


Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.


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