Management of acute coronary syndrome

Author(s):  
Keith A.A. Fox ◽  
Rajesh K. Kharbanda

The acute coronary syndrome (ACS) is precipitated by an abrupt change in an atheromatous plaque, resulting in increased obstruction to perfusion and ischaemia or infarction in the territory supplied by the affected vessel. The clinical consequences of plaque rupture can range from an entirely silent episode, through to unstable symptoms of ischaemia without infarction, to profound ischaemia complicated by progressive infarction, heart failure, and risk of sudden death. Clinical presentation with an ACS identifies a patient at high risk of further cardiovascular events requiring a defined acute and long-term management strategy....

2020 ◽  
pp. 3626-3655
Author(s):  
Rajesh K. Kharbanda ◽  
Keith A.A. Fox

Acute coronary syndrome (ACS) is precipitated by an abrupt change in an atheromatous plaque and/or thrombotic occlusion. This results in increased obstruction to perfusion and ischaemia or infarction in the territory supplied by the affected vessel. The clinical consequences of plaque rupture can range from a clinically silent episode, through to unstable symptoms of ischaemia without infarction, to profound ischaemia complicated by progressive infarction, heart failure, arrhythmia, and risk of sudden death. Clinical presentation with an ACS identifies a patient at high risk of further cardiovascular events requiring a defined acute and long-term management strategy. Prompt relief of pain is important, not only for humanitarian reasons, but also because pain is associated with sympathetic activation, vasoconstriction, and increased myocardial work. The management of prehospital cardiac arrest requires special attention: at least as many lives can be saved by prompt resuscitation and defibrillation as by reperfusion.


Angiology ◽  
2020 ◽  
Vol 71 (9) ◽  
pp. 831-839
Author(s):  
Nuccia Morici ◽  
Valentina Molinari ◽  
Silvia Cantoni ◽  
Andrea Rubboli ◽  
Laura Antolini ◽  
...  

Individual parameters of complete blood count (CBC) have been associated with worse outcome in patients with acute coronary syndrome (ACS). However, the prognostic role of CBC taken as a whole has never been evaluated for long-term incidence of major adverse cardiovascular events (MACEs). Patients were grouped according to their hematopoietic cells’ inflammatory response at different time points during hospital stay. Patients with admission white blood cell count >10 × 109/L, discharge hemoglobin <120 g/L, and discharge platelet count >250 × 109/L were defined as “high-risk CBC.” Among 1076 patients with ACS discharged alive, 129 (12%) had a “high-risk CBC” and 947 (88%) had a “low-risk CBC.” Patients with “high-risk CBC” were older and had more comorbidities. Over a median follow-up of 665 days, they experienced a higher incidence of MACE compared to “low-risk CBC” patients (18.6% vs 8.1%). After adjustment for age, age-adjusted Charlson comorbidity index, female sex, cardiac arrest, suboptimal discharge therapy, coronary artery bypass, and ejection fraction, a high-risk CBC was significantly associated with increased MACE occurrence (adjusted hazard ratio 1.80; 95% CI: 1.09-3.00). The CBC was a prognostic marker in patients with ACS, and its evaluation at admission and discharge could better classify patient’s risk and improve therapeutic management.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J M Garcia Acuna ◽  
A Cordero Fort ◽  
A Martinez ◽  
P Antunez ◽  
M Perez Dominguez ◽  
...  

Abstract The new European Society of Cardiology guideline for ST-segment elevation myocardial infarction recommends that left and right bundle branch block should be considered equal for recommending urgent angiography in patients with suspected myocardial infarction. This consideration is not taken into account in the management of patients with coronary syndrome without ST elevation (NSTEMI). We evaluate the evolution of patients with acute coronary syndrome and long-term bundle branch block. Patients and methods We included 8771 patients admitted to two tertiary hospitals between 2003 and 2017 with an acute coronary syndrome, 5673 NSTEMI (64.3%) and 3098 STEMI (35.7%). All patients had an ECG recorded immediately upon admission. Patients were classified as having right bundle branch block (RBBB), left bundle branch block (LBBB). Long-term follow-up was performed (median 55 months) to assess mortality. Results A total of 8771 patients were included with a mean age of 66.1 years, 72.5% males, 4.1% (362) with LBBB and 5% (440) with RBBB. Patients with BBB were older, with more previous history of myocardial infarction and coronary revascularization and higher prevalence of cardiovascular risk factors. Medical treatment was similar but they were less often submitted to angioplasty. During the acute phase, patients with RBBB and LBBB presented a higher rate of heart failure than those without branch block (4.8% vs 9.1% vs 3.5%, p=0.0001); higher mortality (8.4% vs 10.5% vs 3.0%, p=0.0001); higher stroke rate (2.5% vs 1.4% vs 0.8%, p=0.001); higher rate of renal failure (8.2% vs 9.7% vs 3.9%, p=0.0001) and higher rate of reinfarction (3.0% vs 4.1% vs 1.7%, p=0.001). Patients who had a RBBB or an LBBB had a worse prognosis throughout the follow-up. Heart failure was present in 17.7% of the group with RBBB, 29.6% of LBBB and 11% in the group without branch block (p=0.0001). Mortality during follow-up was 31% in RBBB, 40.6% in LBBB and 18.7% without branch block (p=0.0001). In multivariate analysis of Cox, both RBBB (HR 1.55, 95% CI 1.23–1.98, p=0.0001) and LBBB (HR 1.48, 95% CI 1.22–1.53, p=0.001) were an independent predictors of all-cause mortality (adjustment for GRACE score, gender, treatment with betablockers, angiotensin conversor enzym inhibitors, statin and coronary revascularization). Cox regression model multivariate Conclusions The presence of RBBB or LBBB in the ECG of patients with an ACS is associated with a worse prognosis both during the hospital phase and in the long term. In addition, both bundle branch blocks are independent predictors of long-term mortality in patients with ACS.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O M Peiro Ibanez ◽  
J Ordonez ◽  
A Garcia ◽  
G Bonet ◽  
V Quintern ◽  
...  

Abstract Introduction Biomarkers plays a critical role in diagnostic, prognostication, and decision-making in cardiovascular medicine. Growth differentiation factor-15 (GDF-15) has been reported as a potential biomarker in acute coronary syndrome (ACS). However, there is limited data on the long-term prognostic value after an ACS. Purpose To study the long-term prognostic value of GDF-15 in ACS. Methods We included patients with ACS who underwent coronary angiography. During angiography an arterial blood sample was collected. Plasma GDF-15 were measured and clinical data and long-term events were obtained. As previously reported, risk categories were defined as low risk (<1200ng/L), intermediate (1200–1800ng/L) and high risk (>1800ng/L). Incremental prognostic value of GDF-15 for all-cause death was assessed on top of a clinical model (GRACE score, LVEF<40% and age). Results A total of 358 patients were included; 157 as a low risk, 85 as an intermediate and 116 as a high risk. The median (IQR) age was 65 (56–74) years and 27.4% were female. Of all patients, 61.5% were admitted with non-ST-elevation myocardial infarction, 24.0% with ST-elevation myocardial infarction and 14.5% with unstable angina. Higher values of GDF-15 were consistently associated with an increased prevalence of cardiovascular risk factors. During 6 years of follow-up 54 patients died. Of those patients, 7 (4.5%) had values of GDF-15 below 1200ng/L, 6 (7.1%) between 1200–1800ng/L and 41 (35.3%) above 1800ng/L. After adjustment for a multivariate Cox regression model, GDF-15 >1800ng/L were independently associated with all-cause death (HR 4.5; 95% CI 1.8–11.6; p=0.002) and the composite of major adverse cardiovascular events (MACE) which were identified as all-cause death, nonfatal MI and heart failure (HR 2.5; 95% CI 1.4–4.4; p=0.001). For long-term all-cause death a significant increase of the c-statistic was seen after addition of GDF-15 to the clinical model 0.871 (95% CI 0.817–0.924; p=0.019) as well as net reclassification improvement (0.769; 95% CI 0.487–1.051; p<0.001) and integrated discrimination improvement (0.117; 95% CI 0.062–0.172; p<0.001). Of 18 events of heart failure, 17 occurred in patients with GDF>1800ng/L. A multivariate competing risk model showed a significant association between GDF-15>1800ng/L and incidence of heart failure (adjusted HR 30.8; 95% CI 4.1–231.5; p=0.001) but non-significant association were found for myocardial infarction. KM figures and all-cause death ROC curve Conclusions In the setting of ACS GDF-15 can predict long-term all-cause death, MACE and heart failure and provides incremental prognostic value beyond traditional risks factors in the long-term all-cause death.


2007 ◽  
Vol 53 (12) ◽  
pp. 2112-2118 ◽  
Author(s):  
Peter A Kavsak ◽  
Dennis T Ko ◽  
Alice M Newman ◽  
Glenn E Palomaki ◽  
Viliam Lustig ◽  
...  

Abstract Background: Inflammation in acute coronary syndrome (ACS) can identify those at greater long-term risks for heart failure (HF) and death. The present study assessed the performance of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1) (cytokines involved in the activation and recruitment of leukocytes) in addition to known biomarkers [e.g., N-terminal pro-brain natriuretic peptide (NT-proBNP)] for predicting HF and death in an ACS population. Methods: In a cohort of 216 ACS patients, NT-proBNP (Elecsys®; Roche) and IL-6, IL-8, and MCP-1 (evidence investigator™; Randox) were measured in serial specimens collected early after symptom onset (n = 723). We collected at least 2 specimens from each participant: an early specimen (median 2 h; interquartile range 2–4 h) and a later specimen (9 h; 9–9 h), and used the later specimens’ biomarker concentrations for risk stratification. Results: An increase in both IL-6 and NT-proBNP was observed but not for IL-8 or MCP-1 early after pain onset. Kaplan–Meier analysis demonstrated that individuals with increased NT-proBNP (&gt;183 ng/L) or cytokines (IL-6 &gt; 6.4 ng/L; above upper limit of normal for IL-8 or MCP-1) had a greater probability of death or HF in the following 8 years (P &lt;0.05). In a Cox proportional hazard model adjusted for both CRP and troponin I, increased IL-6, MCP-1, and NT-proBNP remained significant risk factors. Combining all 3 biomarkers resulted in a higher likelihood ratio for death or HF than models restricted to any 2 of these biomarkers. Conclusion: IL-6, MCP-1, and NT-proBNP are independent predictors of long-term risk of death or HF, highlighting the importance of identifying leukocyte activation and recruitment in ACS patients.


2014 ◽  
Vol 25 (4) ◽  
pp. 330-338 ◽  
Author(s):  
Hussam F. AlFaleh ◽  
Khalid F. AlHabib ◽  
Tarek Kashour ◽  
Anhar Ullah ◽  
Alawi A. AlsheikhAli ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Proietti ◽  
C Laroche ◽  
A Tello-Montoliu ◽  
R Lenarczyk ◽  
G A Dan ◽  
...  

Abstract Introduction Heart failure (HF) is a well-known risk factor for atrial fibrillation (AF). Moreover, HF is associated with worse clinical outcomes in patients with known AF. Recently, phenotypes of HF have been redefined according to the level of ejection fraction (EF). New data are needed to understand if a differential risk for outcomes exists according to the new phenotypes' definitions. Purpose To evaluate the risk of major adverse outcomes in patients with AF and HF according to HF clinical phenotypes. Methods We performed a subgroup analysis of AF patients enrolled in the EORP-AF Long-Term General Registry with a history of HF at baseline, available EF and follow-up data. Patients were categorized as follows: i) EF<40%, i.e. HF reduced EF [HFrEF]; ii) EF 40–49%, i.e. HF mid-range EF [HFmrEF]; iii) EF ≥50%, i.e. HF preserved EF [HFpEF]. Any thromboembolic event (TE)/acute coronary syndrome (ACS)/cardiovascular (CV) death, CV death and all-cause death were recorded. Results A total of 3409 patients were included in this analysis: of these, 907 (26.6%) had HFrEF, 779 (22.9%) had HFmrEF and 1723 (50.5%) had HFpEF. An increasing proportion with CHA2DS2-VASc ≥2 was found across the three groups: 90.4% in HFrEF, 94.6% in HFmrEF and 97.3% in HFpEF (p<0.001), while lower proportions of HAS-BLED ≥3 were seen (28.0% in HFrEF, 26.3% in HFmrEF and 23.6% in HFpEF, p=0.035). At discharge patients with HFpEF were less likely treated with antiplatelet drugs (22.0%) compared to other classes and were less prescribed with vitamin K antagonists (VKA) (57.0%) and with any oral anticoagulant (OAC) (85.7%). No differences were found in terms of non-vitamin K antagonist oral anticoagulant use. At 1-year follow-up, a progressively lower rate for all study outcomes (all p<0.001), with an increasing cumulative survival, was found across the three groups, with patients with HFpEF having better survival (all p<0.0001 for Kaplan-Meier curves). After full adjustment, Cox regression analysis showed that compared to HFrEF, HFmrEF and HFpEF were associated with risk of all study outcomes (Table). Cox Regression Analysis HR (95% CI) Any TE/ACS/CV Death CV Death All-Cause Death HFmrEF 0.65 (0.49–0.86) 0.53 (0.38–0.74) 0.55 (0.41–0.74) HFpEF 0.50 (0.39–0.64) 0.42 (0.31–0.56) 0.45 (0.35–0.59) ACS = Acute Coronary Syndrome; CI = Confidence Interval; CV = Cardiovascular; EF = Ejection Fraction; HF = Heart Failure; HR = Hazard Ratio. Conclusions In this cohort of AF patients with HF, HFpEF was the most common phenotype, being associated with a profile related to an increased thromboembolic risk. Compared to HFrEF, both HFmrEF and HFpEF were associated with a lower risk of all major adverse outcomes in AF patients.


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