Left ventricular sphericity index predicts systolic dysfunction in rats with experimental aortic regurgitation

2014 ◽  
Vol 116 (10) ◽  
pp. 1259-1262 ◽  
Author(s):  
Meliza Goi Roscani ◽  
Bertha Fulan Polegato ◽  
Suzana Erico Tanni Minamoto ◽  
Ana Paula Mena Lousada ◽  
Marcos Minicucci ◽  
...  
Keyword(s):  
Aortic Regurgitation ◽  
Sham Group ◽  
Systolic Dysfunction ◽  
Multiple Regression Model ◽  
Left Ventricular ◽  
Sham Operation ◽  
Sphericity Index ◽  
Male Wistar Rats ◽  
Fractional Shortening

Although an increased left ventricular (LV) diastolic diameter (DD) and a decreased ejection fraction have been used as markers for the surgical replacement of an insufficient aortic valve, these signals may be observed when irreversible myocardium damage has already occurred. The aim of this study was to determine whether change in LV geometry predicts systolic dysfunction in experimental aortic regurgitation. Male Wistar rats underwent surgical acute aorta regurgitation (aorta regurgitation group; n = 23) or a sham operation (sham group; n = 12). After the procedure, serial transthoracic echocardiograms were performed at 1, 4, 8, and 16 wk. At the end of protocol, the LV, lungs, and liver were dissected and weighed. During the follow-up, no animal developed overt heart failure. There was a correlation between the LV sphericity index and reduced fractional shortening ( P < 0.001) over time. A multiple regression model showed that the LVDD-sphericity index association at 8 wk was a better predictor of decreased fractional shortening at week 16 ( R2 = 0.50; P < 0.001) than was the LVDD alone ( R2 = 0.39; P = 0.001). LV geometry associated with increased LVDD improved the prediction of systolic dysfunction in experimental aortic regurgitation.

Left ventricular diastolic and systolic performance during chronic experimental aortic regurgitation

1992 ◽  
Vol 263 (1) ◽  
pp. H226-H233 ◽  
Author(s):  
N. M. Magid ◽  
D. C. Wallerson ◽  
J. S. Borer ◽  
A. Mukherjee ◽  
M. S. Young ◽  
...  
Keyword(s):  
Aortic Regurgitation ◽  
Time Course ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Sham Operation ◽  
Functional Responses ◽  
Volume Load ◽  
Systolic Performance ◽  
Chronic Aortic Regurgitation

To study the time course of left ventricular structural and functional responses to chronic aortic regurgitation, aortic regurgitation was surgically induced in rabbits, and Doppler echocardiography was performed preoperatively and serially postoperatively for up to 2.5 yr. Twenty-five New Zealand White rabbits underwent surgical induction of aortic regurgitation and 13 control animals underwent sham operation. Left ventricular endocardial and epicardial surfaces were digitized from M-mode echocardiograms to measure the rates of change of cavity dimensions and wall thicknesses during diastolic relaxation and systolic contraction. Aortic regurgitant animals developed left ventricular dilatation and eccentric hypertrophy that remained relatively stable throughout the follow-up period. Compared with baseline values, left ventricular mass increased 120% and left ventricular internal dimension at end diastole increased 40%, whereas posterior wall thickness at end diastole and fractional shortening remained relatively stable. Left ventricular diastolic performance was enhanced at 6 mo after operation, a finding associated with increased volume load and heart rate following induction of aortic regurgitation. Diastolic performance was then reduced at 12 mo after operation and demonstrated no further decline throughout the remainder of the follow-up period. In contrast, left ventricular systolic performance was not altered following operation and remained preserved until the final assessment at up to 2.5 yr. Thus alterations in diastolic performance occurred without impairment of systolic performance during long-term follow-up of chronic experimental aortic regurgitation.

Heart failure due to chronic experimental aortic regurgitation

1994 ◽  
Vol 267 (2) ◽  
pp. H556-H562 ◽  
Author(s):  
N. M. Magid ◽  
G. Opio ◽  
D. C. Wallerson ◽  
M. S. Young ◽  
J. S. Borer
Keyword(s):  
Heart Failure ◽  
Aortic Regurgitation ◽  
Systolic Dysfunction ◽  
Disease Process ◽  
Experimental Models ◽  
Left Ventricular ◽  
Sham Operation ◽  
Systolic Performance ◽  
Baseline Values ◽  
Chronic Aortic Regurgitation

Previously reported experimental models of aortic regurgitation generally have manifested normal systolic performance and have not developed heart failure [Magid et al. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H226–H233, 1992]. To determine whether more severe chronic experimental aortic regurgitation would generate systolic malperformance, heart failure, and emulate the human disease process, 11 New Zealand White rabbits underwent surgical induction of aortic regurgitation and 5 control animals underwent sham operation. Doppler echocardiography was performed serially for up to 3 yr, and pathological studies were performed at necropsy. Left ventricular internal dimension at end diastole increased 80% (P < 0.00002) and left ventricular weight increased 250% (P < 0.0002) in aortic regurgitant rabbits (regurgitant fraction 52 +/- 13%) compared with baseline values. Six of 11 aortic regurgitant animals died with pathological evidence of congestive heart failure at 1.5 +/- 0.8 yr postoperatively; 2 of these developed severe systolic malperformance, manifest as fractional shortenings of 15 and 19% at 1.6 and 1.7 yr, respectively. Five of 11 aortic regurgitant animals survived until killed at 2.9 +/- 0.1 yr. Thus moderate-to-severe chronic aortic regurgitation in rabbits frequently results in heart failure and systolic dysfunction and may usefully model chronic aortic regurgitation and heart failure in humans.

Atypical Takotsubo Cardiomyopathy with Hypokinetic Left Mid-ventricle and Apical Wall Sparing: A Case Report and Literature Review

2020 ◽  
Vol 16 (3) ◽  
pp. 241-246
Author(s):  
Dipesh Ludhwani ◽  
Belaal Sheikh ◽  
Vasu K Patel ◽  
Khushali Jhaveri ◽  
Mohammad Kizilbash ◽  
...  
Keyword(s):  
Case Report ◽  
Takotsubo Cardiomyopathy ◽  
Systolic Dysfunction ◽  
Obstructive Coronary Artery Disease ◽  
Left Ventricular ◽  
Reduced Ejection Fraction ◽  
Coronary Syndrome ◽  
Normal Left Ventricular ◽  
Artery Disease

Background: Takotsubo Cardiomyopathy (TTC) is an uncommon cause of acute reversible ventricular systolic dysfunction in the absence of obstructive Coronary Artery Disease (CAD). Typically manifesting as apical wall ballooning, TTC can rarely present atypically with apical wall sparing. Case report: A 62-year-old female presented with complaints of chest pain and features mimicking acute coronary syndrome. Coronary angiogram revealed no obstructive CAD and left ventriculogram showed reduced ejection fraction, normal left ventricular apex and hypokinetic mid-ventricles consistent with atypical TTC. The patient was discharged home on heart failure medications and a follow-up transthoracic echocardiogram demonstrated improved left ventricular function with no wall motion abnormality. Conclusion: This case report provides an insight into the diagnosis and management of TTC in the absence of pathognomic features.

scholarly journals AB0422 LEFT VENTRICULAR ABNORMALITIES IN SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS FOLLOWED BY SEQUENTIAL ECHOCARDIOGRAPHY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1510.1-1511
Author(s):  
T. Kuga ◽  
M. Matsushita ◽  
K. Tada ◽  
K. Yamaji ◽  
N. Tamura
Keyword(s):  
Lupus Erythematosus ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Monocyte Count ◽  
Lv Dysfunction ◽  
Group A ◽  
Group B ◽  
Lv Diastolic Dysfunction ◽  
Group D

Background:Cardiovascular disease (CVD) is detected in up to 50% of systemic lupus erythematosus (SLE) patients1and major cause of death2. Even clinically silent SLE patients can develop left ventricular (LV) diastolic dysfunction3. Proper echocardiographic follow up of SLE patients is required.Objectives:To clarify how the prevalence of LV abnormalities changes over follow-up period and identify the associated clinical factors, useful in suspecting LV abnormalities.Methods:29 SLE patients (24 females and 5 men, mean age 52.8±16.3 years, mean disease duration 17.6±14.5 years) were enrolled. All of them underwent echocardiography as the baseline examination and reexamined over more than a year of follow-up period(mean 1075±480 days) from Jan 2014 to Sep 2019. Patients complicated with pulmonary artery hypertension, deep venous thrombosis or pulmonary embolism and underwent cardiac surgery during the follow-up period were excluded. Left ventricular(LV) systolic dysfunction was defined as ejection fraction (EF) < 50%. LV diastolic dysfunction was defined according to ASE/EACVI guideline4. LV dysfunction (LVD) includes one or both of LV systolic dysfunction and LV diastolic function. Monocyte to HDL ratio (MHR) was calculated by dividing monocyte count with HDL-C level.Prevalence of left ventricular abnormalities was analysed at baseline and follow-up examination. Clinical characteristics and laboratory data were compared among patient groups as follows; patients with LV dysfunction (Group A) and without LV dysfunction (Group B) at the follow-up echocardiography, patients with LV asynergy at any point of examination (Group C) and patients free of LV abnormalities during the follow-up period (Group D).Results:At the baseline examination, LV dysfunction (5/29 cases, 13.8%), LV asynergy (6/29 cases, 21.7%) were detected. Pericarditis was detected in 7 patients (24.1%, LVD in 3 patients, LV asynergy in 2 patients) and 2 of them with subacute onset had progressive LV dysfunction, while 5 patients were normal in echocardiography after remission induction therapy for SLE. At the follow-up examination, LV dysfunction (9/29 cases, 31.0%, 5 new-onset and 1 improved case), LV asynergy (6/29 cases, 21.7%, 2 new-onset and 2 improved cases) were detected. Though any significant differences were observed between Group A and Group B at the baseline, platelet count (156.0 vs 207.0, p=0.049) were significantly lower in LV dysfunction group (Group A) at the follow-up examination. Group C patients had significantly higher uric acid (p=0.004), monocyte count (p=0.009), and MHR (p=0.003) than Group D(results in table).Conclusion:LV dysfunction is progressive in most of patients and requires regular follow-up once they developed. Uric acid, monocyte count and MHR are elevated in SLE patients with LV asynergy. Since MHR elevation was reported as useful marker of endothelial dysfunction5, our future goal is to analyse involvement of monocyte activation and endothelial dysfunction in LV asynergy of SLE patients.References:[1]Doria A et al. Lupus. 2005;14(9):683-6.[2]Manger K et al. Ann Rheum Dis. 2002 Dec;61(12):1065-70.[3]Leone P et al. Clin Exp Med. 2019 Dec 17.[4]Nagueh SF et al. J Am Soc Echocardiogr. 2016 Apr;29(4):277-314.[5]Acikgoz N et al. Angiology. 2018 Jan;69(1):65-70.Numbers are median (interquartile range), Mann-Whitney u test were performed, p value less than 0.05 was considered statistically significant.Disclosure of Interests: :None declared

Non-compaction cardiomyopathy: genetic and clinical features, 5-years outcomes

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Vaikhanskaya ◽  
L.N Sivitskaya ◽  
A.D Liaudanski ◽  
N.G Danilenko ◽  
O.G Davydenko
Keyword(s):  
Predictive Model ◽  
Myocardial Fibrosis ◽  
Systolic Dysfunction ◽  
Ventricular Tachyarrhythmia ◽  
Neuromuscular Disorder ◽  
Left Ventricular ◽  
Adverse Outcomes ◽  
Successful Resuscitation ◽  
Morphological Criteria

Abstract   Presence of morphological sign as a left ventricular non-compaction (LVNC) only, without supporting clinical criteria, does not determine diagnosis of non-compaction cardiomyopathy (NCCM). Objective To study of the spectrum of NCCM-associated genes, analysis of phenotype-genotype correlations and predictors of life-threatening ventricular tachyarrhythmia (ltVTA), myocardial fibrosis, and adverse outcome. Methods Of 93 pts with identified (Echo/MRI) morphological criteria for LVNC (follow-up median 5,1 years), 60 unrelated pts were included in the study (aged 38.5±13.8 years; 33/55% male; LVEF 42.1±12.9%) with clinical confirmed NCCM (presence any one obligate criteria): family history, neuromuscular disorder, abnormal 12-lead ECG, arrhythmia, HF or thromboembolism (Figure). Genetic testing by NGS (174 genes) was performed; all variants considered as pathogenic (PV) and likely pathogenic (LPV) were confirmed by a Sanger sequencing. Baseline and follow-up data (ECG, HM, Echo, MRI, device interrogation) were collected. Combined adverse outcomes (HF death; SCD; LVAD; HTx; and ltVTA: VT/VF, successful resuscitation, ICD shock) were accepted as composite endpoint. Results PV and LPV were detected in 33 (55%) pts. The most common variants were identified in sarcomere genes – TTNtv, MYBPC3, and MYH7 (47.4%); ion channel genes – 18.2%; digenic mutations were found in 21.6% pts. Gene positivity was associated with systolic dysfunction (LVEF≤49%); the highest risk of low LVEF revealed for digenic carriers (OR 38; 95% CI 4.74–305; p=0.0001). According to CATREG analysis, predictive model was built (R=0,80; R2=0,65; F=10,1; p=0,0001); the presence of disease-causing PV/LPV (β=0.46; F=15.2; p=0,0001) along with low LVEF (β=−0.28; F= 5.96; p=0,018), fibrosis (β=0.21; F= 3.05; p=0,037), wide QRS (β=0.22; F= 4.11; p=0,011) were identified as independent predictors of adverse outcomes. As a result of ROC analysis, independent predictors of ltVTA were determined: fibrosis (nLGE≥2: AUC 0.824; 95% CI: 0.716–0.931; p=0.0001; sen 69%, spe 79%), systolic dysfunction (LVEF≤39%: AUC 0.832; 95% CI: 0.720–0.943; p=0.0001; sen 85%, spe 70%) and nsVT (HR≥150 bmp: AUC 0.829; 95% CI: 0.719–0.940; p=0.0001; sen 76%, spe 83%). According to ROC curves analysis, independent markers of myocardial fibrosis (LGE) were found: nsVT (HR≥150 bpm: AUC 0.766; 95% CI: 0.635–0.897; sen 80%, spe 77%); QRS fragmentation (nQRSfr≥4 leads ECG: AUC 0.822; 95% CI: 0.706–0.938; sen 76%, spe 92%); QTc duration (QTc≥450 ms: AUC 0.828; 95% CI: 0.722–0.935; sen 80%, spe 72%) and native MRI T1-relaxation (T1≥1086 ms: AUC 0.752; 95% CI: 0.626–0.879; sen 70%, spe 70%). Conclusion This results show a basically genetic causing NCCM with predominant mutations in sarcomere genes. As per predictive model, the strongest predictor of poor outcome was gene positivity. Identifying the genetic cause allows risk stratification and management optimization with counseling NCCM pts and their relatives. Study design Funding Acknowledgement Type of funding source: None

Abstract 5920: Usefulness of Late Gadolinium Enhancement as Non-invasive Arrhythmic Risk Marker in Patients with Heart Failure and Systolic Dysfunction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Alfonso Valle ◽  
Mercedes Nadal ◽  
Jordi Estornell ◽  
Nieves Martinez ◽  
Miguel Corbi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Late Gadolinium Enhancement ◽  
Risk Stratification ◽  
Systolic Dysfunction ◽  
Total Mortality ◽  
Left Ventricular ◽  
Gadolinium Enhancement ◽  
Non Invasive ◽  
Patients With Heart Failure

The identification of prognostic markers in patients with heart failure of both ischemic and non ischemic etiology is an increasing need in the era of devices therapy. Risk stratification for sudden cardiac death (SCD) remains problematic with reliance on left ventricular function which predicts total mortality rather than arrhythmic events (AE). Recently cardiac magnetic resonance was employed to predict susceptibility for malignant arrhythmias. This study sought to determine the utility of late gadolinium enhancement (LGE) to predict AE. Three hundred consecutive patients with symptomatic heart failure and systolic dysfunction of both ischemic and non ischemic cause undergoing CMR, were classified into two groups attending to the presence (n 160) or absence of LGE (n 140), and were followed prospectively during 842 days. The primary endpoint was the combined of SCD or Ventricular tachycardia (VT). 23 patients had AE (8 SCD/15 VT) during the follow-up, 19 of them presenting LGE (83%). The presence of LGE was associated to a significantly higher AE rate (11.8.% vs 2.8% p< 0.001)(figure ). Compared to patients without LGE, midwall fibrosis and an ischemic pattern of LGE predicted AE. (3% vs 5% vs 14%, p= 0.001) LGE is a new non-invasive predictor of AE in patients with heart failure and systolic dysfunction. This suggest a potential role for risk stratification and better selection of patients who needs device therapy

Abstract 18294: Left Ventricular Systolic Dysfunction Early After Resuscitation From Cardiac Arrest is Associated With Shockable Arrest Rhythm

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Jacob C Jentzer ◽  
Hussein Abu-Daya ◽  
Asher Shafton ◽  
Meshe Chonde ◽  
Didier Chalhoub ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Hospital Mortality ◽  
Troponin I ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Mitral Annulus ◽  
Left Ventricular ◽  
Ventricular Systolic Dysfunction ◽  
Mitral Annulus Velocity ◽  
Fractional Shortening

Introduction: Left ventricular systolic dysfunction (LVSD) is common after resuscitation from cardiac arrest (CA). The association of echocardiographic LVSD with cardiac rhythm during CA is not well described. Hypothesis: Patients with a shockable rhythm (VT/VF) will have a greater degree of LVSD by echocardiography after CA. Methods: Prospective registry of patients resuscitated from CA underwent transthoracic echocardiography (TTE) within 24 hours after CA. We determined 2D measurements, LVEF, spectral Doppler of mitral inflow and LV outflow, systolic and diastolic tissue Doppler of the mitral annulus velocity, and tricuspid plane annular excursion (TAPSE). We collected data on in-hospital mortality as well as vasopressor doses and troponin I levels. TTE parameters and clinical characteristics were compared between patients with a shockable (VT/VF) arrest rhythm and a non-shockable (asystole/PEA) arrest rhythm and between survivors and non-survivors using t-tests and ANOVA. Results: Of the 55 patients, the 23 (42%) with shockable CA rhythms had significantly higher LV end-systolic dimension (4.1cm vs. 3.3cm, p = 0.0073), lower LV fractional shortening (0.15 vs. 0.28, p <0.0001), and lower LVEF both by visual estimate (36.2% vs. 52.3%, p = 0.0012) and by Simpson’s biplane method (37.5% vs. 52.3%, p = 0.0506). Other measured TTE parameters did not differ between groups, including TAPSE (shockable 1.53 vs. non-shockable 1.82, p = 0.1731). Admission and peak 24 hour vasopressor requirements did not differ between groups. Peak troponin levels were higher (22.26 vs. 3.88, p = 0.0198) in patients with shockable CA rhythms, but admission troponin levels were no different (0.88 vs. 0.51, p = 0.1527). TTE parameters did not differ between survivors and non-survivors (visual LVEF 47.0% vs. 44.2%, p = 0.5968; LV fractional shortening 0.19 vs. 0.25, p = 0.0916). Conclusions: Patients with shockable CA rhythms have more severe LVSD on 24 hour echocardiography despite similar vasopressor requirements and admission troponin levels. Echocardiographic parameters at 24 hours did not predict in-hospital mortality. Early echocardiography after CA appears more useful for differentiating primary CA rhythm than for predicting mortality.

P1868Risk of arrhythmias after myocardial infarction in patients with left ventricular systolic dysfunction according to mode of revascularization: a CARISMA substudy

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Thomsen ◽  
S Pedersen ◽  
P K Jacobsen ◽  
H V Huikuri ◽  
P E Bloch Thomsen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Loop Recorder ◽  
Ventricular Ejection Fraction ◽  
New Onset

Abstract Introduction The CARISMA trial was the first study to use continuous monitoring for documentation of long-term arrhythmias in post-infarction patients with left ventricular dysfunction. During the study duration (2000–2005), primary PCI (pPCI) as treatment of acute myocardial infarction was introduced approximately midway (2002) on the enrolling centres. Purpose The aim of this study was to describe the influence of mode of revascularization after myocardial infarction (AMI) on long-term risk of risk of new onset atrial fibrillation, ventricular tachyarrhythmias and brady arrhythmias. Methods The study is a sub-study on the CARISMA study population that consisted of patients with AMI and left ventricular ejection fraction ≤40%, which received an implantable loop recorder and was followed for 2 years. After exclusion of 15 patients who refused device implantation and 26 with pre-existing arrhythmias, 268 of the 312 patients were included. Choice of revascularization was made by the treating team independently of the trial and was retrospectively divided into primary percutaneous intervention (pPCI), subacute PCI (24 hours to 2 weeks after AMI), primary thrombolysis or no revascularization. Endpoints were new-onset of arrhythmias and major cardiovascular events (MACE). The Kaplan-Meier (figure 1) and Mantel-Byar methods were used for time to first event risk analysis. Results A total of 77 patients received no revascularization, whereas 49 received thrombolysis only and 142 received PCI. At two-years follow up patients treated with any PCI had a significant lower risk (0.40, n=63) of any arrhythmia compared to patients treated with trombolysis (0.60, n=30) or no revascularization (0.68, n=16) (p<0.001, unadjusted) (figure 1). Risk of MACE was significant higher in patients with any arrhythmia (0.25, n=76) compared to no arrhythmia (0.11, n=93) at two years follow-up (p=0.004, unadjusted). Figure 1 Conclusion(s) The long-term risk of new onset arrhythmias after AMI was significantly lower in patients treated with any PCI compared to patients not revascularized or treated with thrombolysis. Risk of MACE was significantly higher in patients with new onset arrhythmias compared to patients with no arrhythmias.

scholarly journals Enhanced Inflammation is a Marker for Risk of Post-Infarct Ventricular Dysfunction and Heart Failure

2020 ◽  
Vol 21 (3) ◽  
pp. 807 ◽  
Author(s):  
Iwona Świątkiewicz ◽  
Przemysław Magielski ◽  
Jacek Kubica ◽  
Adena Zadourian ◽  
Anthony N. DeMaria ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Multivariable Analysis ◽  
High Sensitivity ◽  
Left Ventricular ◽  
St Segment Elevation ◽  
Reactive Protein

Acute ST-segment elevation myocardial infarction (STEMI) activates inflammation that can contribute to left ventricular systolic dysfunction (LVSD) and heart failure (HF). The objective of this study was to examine whether high-sensitivity C-reactive protein (CRP) concentration is predictive of long-term post-infarct LVSD and HF. In 204 patients with a first STEMI, CRP was measured at hospital admission, 24 h (CRP24), discharge (CRPDC), and 1 month after discharge (CRP1M). LVSD at 6 months after discharge (LVSD6M) and hospitalization for HF in long-term multi-year follow-up were prospectively evaluated. LVSD6M occurred in 17.6% of patients. HF hospitalization within a median follow-up of 5.6 years occurred in 45.7% of patients with LVSD6M vs. 4.9% without LVSD6M (p < 0.0001). Compared to patients without LVSD6M, the patients with LVSD6M had higher CRP24 and CRPDC and persistent CRP1M ≥ 2 mg/L. CRP levels were also higher in patients in whom LVSD persisted at 6 months (51% of all patients who had LVSD at discharge upon index STEMI) vs. patients in whom LVSD resolved. In multivariable analysis, CRP24 ≥ 19.67 mg/L improved the prediction of LVSD6M with an increased odds ratio of 1.47 (p < 0.01). Patients with LVSD6M who developed HF had the highest CRP during index STEMI. Elevated CRP concentration during STEMI can serve as a synergistic marker for risk of long-term LVSD and HF.

scholarly journals Diabetic cardiomyopathy: acute and reversible left ventricular systolic dysfunction due to cardiotoxicity of hyperglycaemic hyperosmolar state—a case report†

2019 ◽  
Vol 3 (2) ◽  
Author(s):  
Umut Kocabaş ◽  
Özgür Yılmaz ◽  
Volkan Kurtoğlu
Keyword(s):  
Blood Glucose ◽  
Diabetic Cardiomyopathy ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Blood Glucose Control ◽  
Left Ventricular ◽  
Pathophysiological Mechanism ◽  
Ventricular Systolic Dysfunction ◽  
Arterial Blood

Abstract Background Diabetic cardiomyopathy (DC) is defined as a ventricular diastolic and/or systolic dysfunction, which is directly related to diabetes mellitus (DM) in the absence of coronary artery disease, valvular, congenital or hypertensive heart disease, and alcoholism. In this report, we present an unusual case of a patient with DC and reversible, acute left ventricular systolic dysfunction due to cardiotoxicity of hyperosmolar hyperglycaemic state (HHS). Case summary A 20-year-old male patient presented with weakness and polyuria. Physical examination and electrocardiogram were normal. Laboratory results and arterial blood gas analysis were consistent with HHS. Baseline echocardiography showed global left ventricular hypokinesis with an ejection fraction (EF) of 36%. The patient’s clinical condition improved after blood glucose level normalization and echocardiography revealed progressive improvement in the left ventricular systolic function with an EF of 54% at the 5-day follow-up and an EF of 69% at the 15-day follow-up. Discussion Uncontrolled DM and hyperglycaemic crisis may result in cardiotoxicity, acute left ventricular systolic dysfunction, and DC. The pathophysiological mechanism of this phenomenon is still unclear. Blood glucose control is the most important strategy for the prevention of DC.

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