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.

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.

MO191MANAGEMENT OF HYPERKALAEMIA TO FACILITATE RAASI THERAPY IN PATIENTS WITH HEART FAILURE IN A BESPOKE UK CLINIC

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ibrahim Ali ◽  
Philip A Kalra
Keyword(s):  
Heart Failure ◽  
Serum Potassium ◽  
Left Ventricular Systolic Dysfunction ◽  
Care Pathway ◽  
Beta Blockers ◽  
Angiotensin Receptor Blockers ◽  
Systolic Dysfunction ◽  
Systolic Heart Failure ◽  
Left Ventricular

Abstract Background and Aims Best practice for treatment of patients with chronic heart failure involves beta-blockers and renin-angiotensin-aldosterone system inhibitors (RAASi) such as ACE inhibitors (ACE-i), angiotensin receptor blockers (ARB), mineralocorticoid antagonists (MRA) and neprolysin inhibitor/ARB. However, use of these agents, and optimisation of their dosage, is frequently limited by hyperkalaemia, the incidence of which is increased by the co-prevalence of chronic kidney disease (CKD). Management of patients in a bespoke Hyperkalaemia Clinic can be advantageous in facilitating optimal use of RAASi. Method A Hyperkalaemia Clinic was opened in July 2019 in this tertiary renal centre within an NHS trust that hosts 4 district hospital heart failure services. Referrals of patients with left ventricular systolic dysfunction whose RAASi could not be optimised because of hyperkalaemia were encouraged from heart failure specialist nurses and cardiologists. Management of the patients incorporated commencement of patiromer at 8.4g daily and increases in RAASi was usually devolved to the referring team. This report describes the activity and short-term outcomes of the first 17 months after opening of the clinic (follow up until 1st January 2021). Results 34 patients with systolic heart failure and problems with RAASi-associated hyperkalaemia were referred to the clinic. Mean age was 74 (range 44-88) years, 28% had stage 3a, 28% 3b and 8% stage 4 CKD. ACE-I or ARB were being used in 73% of patients at referral, 73% were using beta blockers and 50% MRA with loop diuretic use in 70%. At first visit 64% had normokalaemia, and 36% serum potassium 5.4-6.0 mmol/L. During follow-up, 6 (18%) patients discontinued patiromer due to gastrointestinal side effects, 3 no longer required the binder because of decrease in RAASi use and 2 patients died (one each from stroke and sepsis). One patient was switched to an alternative potassium binder. As of 1st January 2021, patiromer was still being administered to 22 (65%) patients, 8 of which had received this for &gt;12 months; all patients remained normokalaemic and none of them required magnesium supplementation. An increase in RAASi therapy had occurred in only 12 (35%) patients. Conclusion Our experience demonstrates the relative simplicity of managing hyperkalaemia via a bespoke clinic in cardio-renal patients. As this was nephrology-led, optimised management was dependent upon the assertive and collaborative involvement of the referring heart failure teams who helped with biochemical monitoring and alteration of RAASi therapy. However, less than half of the patients benefitted from an increase in RAASi therapy after normalisation of serum potassium, and there was definitely scope for improving this component of the care pathway via more direct multi-disciplinary interaction with the heart failure teams.

scholarly journals Association of High Sensitive C - Reactive Protein with Severity of the Left Ventricular Systolic Dysfunction in Acute Anterior ST Elevation Myocardial Infarction

2018 ◽  
Vol 44 (2) ◽  
pp. 71-76
Author(s):  
Aparna Rahman ◽  
Abdul Wadud Chowdhury ◽  
Lutfur Rahman Khan ◽  
Khandkar Md. Nurus Sabah ◽  
Mohammad Gaffar Amin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
C Reactive Protein ◽  
Group Iii ◽  
Reactive Protein ◽  
St Elevation ◽  
Hs Crp

High Sensitive C-reactive protein (hs- CRP) is an established risk marker in coronary artery disease. It is a marker of inflammation activated early after Acute Myocardial Infarction (AMI) and its quantity depends upon extent of myocardial damage. Release of inflammatory marker occur after acute myocardial infarction leading to cardiac remodeling which clinically manifests as Heart failure (HF). Heart failure is a common complication after acute anterior myocardial infarction (AMI). The prevalence of post-infarct Left Ventricular Systolic Dysfunction (LVSD) ranges from 27 to 60 % and half of patients having early post-infarct LVSD subsequently develop chronic heart failure. The purpose of this study is to show association between hs-CRP with LVSD in AMI and early detection of HF. This was a cross-sectional analytical study in which hs-CRP was done among all the study subjects between 24-48 hours after onset of AMI. The study population was categorized into groups I, II, II according to the lowest to highest hs-CRP level. Transthoracic echocardiography was done between 24-48 hours of anterior ST Elevation Myocardial Infarction (STEMI). Then LVSD was assessed between those three groups and searched for association. Severely reduced ejection fraction (EF) was found in patients of group III (highest hs-CRP tertile) only. Severe and moderately reduced EF and FS was found significantly more in group III and II than group I (mid and lowest hs-CRP tertile) (p<0.001). High level of hs-CRP in patient of acute anterior STEMI patients was associated with moderate to severe reduction in EF and Fractional Shortening (FS).  So hs- CRP may be a prognostic marker in acute anterior STEMI complicating LVSD and early management would improved the short and long term prognosis.

scholarly journals Titin-Related Dilated Cardiomyopathy: The Clinical Trajectory and the Role of Circulating Biomarkers in the Clinical Assessment

Diagnostics ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 13
Author(s):  
Przemysław Chmielewski ◽  
Grażyna Truszkowska ◽  
Ilona Kowalik ◽  
Małgorzata Rydzanicz ◽  
Ewa Michalak ◽  
...  
Keyword(s):  
Heart Failure ◽  
Risk Assessment ◽  
Dilated Cardiomyopathy ◽  
Troponin T ◽  
Left Ventricular Systolic Dysfunction ◽  
Multivariable Analysis ◽  
Disease Onset ◽  
Left Ventricular ◽  
Cardiac Biomarkers

Titin truncating variants (TTNtv) are known as the leading cause of inherited dilated cardiomyopathy (DCM). Nevertheless, it is unclear whether circulating cardiac biomarkers are helpful in detection and risk assessment. We sought to assess 1) early indicators of cardiotitinopathy including the serum biomarkers high-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in clinically stable patients, and 2) predictors of outcome among TTNtv carriers. Our single-center cohort consisted of 108 TTNtv carriers (including 70 DCM patients) from 43 families. Clinical, laboratory and follow-up data were analyzed. The earliest abnormality was left ventricular dysfunction, present in 8, 26 and 47% of patients in the second, third and fourth decade of life, respectively. It was followed by symptoms of heart failure, linked to NT-proBNP elevation and severe left ventricular systolic dysfunction, and later by arrhythmias. Hs-cTnT serum levels were increased in the late stage of the disease only. During the median follow-up of 5.2 years, both malignant ventricular arrhythmia (MVA) and end-stage heart failure (esHF) occurred in 12% of TTNtv carriers. In multivariable analysis, NT-proBNP level ≥650 pg/mL was the best predictor of both composite endpoints (MVA and esHF) and of MVA alone. In conclusion, echocardiographic abnormalities are the first detectable anomalies in the course of cardiotitinopathies. The assessment of circulating cardiac biomarkers is not useful in the detection of the disease onset but may be helpful in risk assessment.

Mortality and morbidity reduction after frequent premature ventricular complexes ablation in patients with left ventricular systolic dysfunction

EP Europace ◽  
2019 ◽  
Vol 21 (7) ◽  
pp. 1079-1087 ◽  
Author(s):  
Antonio Berruezo ◽  
Diego Penela ◽  
Beatriz Jáuregui ◽  
David Soto-Iglesias ◽  
Luis Aguinaga ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Cardiac Transplantation ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cardiac Mortality ◽  
Ventricular Ejection Fraction

Aims Ablation of frequent premature ventricular complexes (PVCs) improves left ventricular ejection fraction in patients with left ventricular (LV) systolic dysfunction. This study aims to evaluate the long-term hard outcomes and potential prognostic variables in this population. Methods and results Prospective multicentre study including 101 consecutive patients [56 ± 12 years old, 62 (61%) men] with LV systolic dysfunction and frequent PVCs who underwent PVC ablation before November 2015. The last evaluation performed was considered the long-term follow-up (LTFUP) evaluation. Mean follow-up was 34 ± 16 months (range 24–84 months). Ablation was successful in 95 (94%) patients. There was a significant reduction in the PVC burden from 21 ± 12% at baseline to 3.8 ± 6% at LTFUP, P < 0.001. Left ventricular ejection fraction improved from 32 ± 8% at baseline to 39 ± 12% at LTFUP (P < 0.001) and New York Heart Association class from 2.2 ± 0.6% to 1.3 ± 0.6% (P < 0.001). Brain natriuretic peptide levels decreased from 136 (78–321) to 68 (32–144) pg/mL (P = 0.007). Most of this improvement occurs during the first 6 months after ablation. Persistent abolition of at least 18 points of the baseline PVC burden was independently and inversely associated with the composite endpoint of cardiac mortality, cardiac transplantation, or hospitalization for heart failure during follow-up [hazard ratio 0.18 (0.05–0.66), P = 0.01]. Conclusion In patients with LV systolic dysfunction, ablation of frequent PVCs induces a significant improvement in functional, structural, and neurohormonal status, which persists at LTFUP. A sustained reduction in the baseline PVC burden is associated with a lower risk of cardiac mortality, cardiac transplantation, or hospitalization for heart failure during follow-up.

scholarly journals Titin-Related Dilated Cardiomyopathy: The Sequence of Events and The Role of Circulating Biomarkers in The Clinical Assessment

2021 ◽  
Author(s):  
Przemysław Chmielewski ◽  
Grażyna Truszkowska ◽  
Ilona Kowalik ◽  
Małgorzata Rydzanicz ◽  
Ewa Michalak ◽  
...  
Keyword(s):  
Heart Failure ◽  
Risk Assessment ◽  
Dilated Cardiomyopathy ◽  
Troponin T ◽  
Left Ventricular Systolic Dysfunction ◽  
Multivariable Analysis ◽  
Left Ventricular ◽  
Cardiac Biomarkers ◽  
Sequence Of Events

Abstract Titin truncating variants (TTNtv) are known as the leading cause of inherited dilated cardiomyopathy (DCM). Nevertheless, the clinical course is not fully understood and it is unclear whether circulating cardiac biomarkers are helpful in the detection and risk assessment. We sought to assess: 1) early signs of cardiotitinopathy including serum biomarkers: high-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in clinically stable patients, and 2) indicators of outcome among TTNtv carriers. Our single-centre cohort included 108 carriers (including 70 DCM patients) from 43 families. Clinical, laboratory and follow-up data were analyzed. The earliest abnormality was left ventricular dysfunction, present in 8, 26 and 47% of patients in the 2nd, 3rd and 4th decade of life, respectively. It was followed by symptoms of heart failure and elevation of NT-proBNP, linked to severe (persistent or transient) left ventricular systolic dysfunction, and later by arrhythmias, preceding both malignant ventricular arrhythmia (MVA) and end-stage heart failure (esHF). Hs-cTnT serum levels were increased in the late stage of the disease only. During the median follow-up of 5.2 years both MVA and esHF occurred in 12% of TTNtv carriers. In multivariable analysis, NT-proBNP level ≥650 pg/ml was the best predictor of both composite endpoint (MVA and esHF), and of MVA alone. We conclude that assessment of circulating cardiac biomarkers is not useful in the detection of cardiotitinopathies but may be helpful in the risk assessment.

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