RỐI LOẠN NHỊP THẤT trong nhồi máu cơ tim cấp

This variation is largely due to the frequency of recording the cardiac rhythm of patients with acute myocardial infarction.. This variation is largely due to the frequency of recording

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RỐI LOẠN NHỊP THẤT

trong nhồi máu cơ tim cấp

ThS.BS Hoàng Việt Anh Trưởng phòng Q3B - Viện Tim mạch quốc gia Việt Nam

Hà Nội 26/11/2016

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Nhồi máu cơ tim

•  Là bệnh lý tim mạch có tỷ lệ mắc ngày càng tăng và tỷ lệ tử vong cao

•  Tỷ lệ mới mắc tại Hoa Kỳ: 735.000 người/năm

•  Yếu tố nguy cơ: Tăng huyết áp, ĐTĐ2, Rối loạn lipid máu, Béo phì, ít vận động thể chất, cuộc sống căng thẳng…

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Rối loạn nhịp là một biến chứng của NMCT

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FIGURE 1: Avionics’ monitoring system The unit, on the right side of the picture, represents the

scan-ner. The recorder is the small portable unit in the center of the picture. On the left side is the

eLectro-cardiocharter.

520

Cardiac Arrhythmias in Acute Myocardial Infarction

II Incidence of the Common Arrhythmias with Special Reference to Ventricular Tachycardia*

F A. BASHOUR, M.D., F.C.C,P,,** E. JONES, M.D.f AND R EDMONSON, M.D

Dallas, Texas

INTRODUCTION

T HE MORTALITY RATE IN ACUTE

MYO-cardial infarction has changed little

in the past 30 years; it remained in the neighborhood of 30 per cent In the ma- jority of instances, death occurred in the

first 48 hours Approximately in 50 per cent

of these patients, death is sudden and expected These patients are clinically well

un-at the time of death without sufficient

de-struction of myocardial tissue at necropsy

to explain the terminal event, It has been

*From the Department of Medicine, University

of Texas Southwestern Medical School.

**Associate Professor of Medicine.

fPresent address - intern in Medicine at ford University.

Resident in Medicine.

Part of this work was presented at the Texas Heart Association Meeting, Texarkana (Febru- ary 2, 1965) and the Midwestern Section, Amer- ican Federation for Clinical Research, Chicago,

November, l965.’

generally accepted, because of the sequence

of events following the ligation of coronary arteries in dogs, that this group dies of ventricular arrhythmia and fibrillation.

The reported incidence of cardiac

ar-rhythmias varied widely This variation is largely due to the frequency of recording the cardiac rhythm of patients with acute

myocardial infarction The development of

methods for continuous recording of the cardiac rhythm has permitted the study of

the true incidence and the evaluation of the

types of the cardiac arrhythmia that occur

in the immediate post-infarction period.

The purpose of this study was fold: to describe the incidence of the seri- ous cardiac arrhythmia, to correlate the presence of ventricular tachycardia with known clinical features of the disease, and

three-a preliminthree-ary report on the use of

diphenyl-Downloaded From: http://journal.publications.chestnet.org/ on 11/15/2016

520

INTRODUCTION

Stan-ford University.

Heart Association Meeting, Texarkana ary 2, 1965) and the Midwestern Section, Amer- ican Federation for Clinical Research, Chicago,

INCIDENCE OF COMMON ARRHYTHMIAS

Voiume Si, No S

Patients with electrocardiographic dence of an acute myocardial infarction

evi-were studied In group 1, 28 patients with

30 episodes of acute myocardial infarction (referred to below as 30 cases) were moni-

tored for a period of 24 hours In 16 stances, the myocardial lesion was located

diaphragmatic area The onset of the

ap-pearance of the precordial chest pain, or

of the pain in patients with previous sodes of angina pectoris Monitoring of the

after the appearance of the chest pain.

with acute myocardial infarction were given Dilantin prophylactically This group of

MONITORING SYSTEM*

*Manufactured by Avionics Research Corporation, Los Angeles, California.

replacement of the P wave of the normal

Downloaded From: http://journal.publications.chestnet.org/ on 11/15/2016

520

INTRODUCTION

Stan-ford University.

Heart Association Meeting, Texarkana ary 2, 1965) and the Midwestern Section, Amer- ican Federation for Clinical Research, Chicago,

(Febru-November, l965.’

The purpose of this study was

the sinus rhythm was 85/mm and that of the

INCIDENCE OF COMMON ARRHYTHMIAS 523

dine was used alone in one other patient

for atrial arrhythmia.

two groups according to the location of the myocardial infarction: anterior and inferior

involvement of the lateral myocardial wall

depending on whether the anterior or the inferior wall was predominantly involved.

ar-rhythmias are reported in Table 1 Atrial

re-sponse in two patients Wandering maker was observed in 11 patients Prema-

pace-ture atrial beats were frequent in four tients Paroxysmal supraventricular tachy-

pa-cardia occurred in five patients, four of

Multifocal ventricular premature beats were seen in all patients R/T phenomenon was observed in three (two had anterior

and one inferior myocardial infarction) and ventricular bigeminy in 11 patients In one of these, the bigeminal rhythm lasted three hours True ventricular tachycardia was present in 15 patients, and the incidence was equally distributed between anterior and inferior myocardial infarction.

The number of attacks of ventricular cardia varied between one and 70 The ventricular rate ranged between 100 and

tachy-220 beats per minute In five patients, two

or more ventricular foci were responsible

ectopic ventricular rhythm was present in six patients, five of whom had anterior and one inferior myocardial infarction The attacks numbered between one and ten in

a single patient and the ventricular rate ranged between 72 and 90 beats per min-

ute In one patient, both types of ventricular rhythm were present Runs of three pre-

mature ventricular beats interrupted by normally conducted beats were seen in 16 patients; 12 of these patients had runs of

V.nt rot.-721 mm SInUs thythm-$SlmIn.

524

Diseases of

BASHOUR, JONES AND EDMONSON the Chest

TABLE 1-INCIDENCE OF COMMON CARDIAC ARRHYTHMIAS IN 30 CASES OF ACUTE MYOCARDIAL INFARCTION DISTRIBUTED ACCORDING TO THE SITE OF THE MYOCAItDIAL LESION Anterior Inferior Total

No %

Episodes- 16 14 Atrial fibrillation 1 2 3 10 Supraventricular

tachycardia 4 1 5 16.6

Complete AV block 0 3 3 10

Multifocal PVC’s 16 14 30 100 Ectopic ventricular

rhythms:

a) True ventricular tachycardia (rate greater than

than 100/mm) 8 7 15 50 b) Slow ventricular

rhythm (rate from 70-100/mm) 5* 1 6 20

*One patient had both slow and

ventricular rhythms.

rapid ectopic

ventricular tachycardia In one, the run of

three PVC’s was followed by ventricular fibrillation (Fig 4).

The serum glutamic oxaloacetic

trans-aminase (SGOT) levels were determined

in 27 patients The peak rise of SGOT blood levels was correlated with the ap-

pearance of the ectopic ventricular rhythm and reported in Table 2 Patients with the slow ectopic ventricular rhythm had a mean SGOT of 213 units per ml, and those with true ventricular tachycardia 194 units per ml In the absence of ventricular tachycardia, the mean SGOT rise in patients with acute myocardial infarction was 93 units per ml The number of patients with shock or heart failure on admission is small

to demonstrate a close relationship between these clinical features and the appearance

of ectopic ventricular rhythms.

Dilantin was used prophylactically in 14 consecutive patients The abnormalities in the cardiac arrhythmias encountered in this group are reported in Table 3 Multifocal premature ventricular beats were observed

in 13 patients and ventricular bigeminy in three The premature ventricular beats, although multifocal, were quite reduced in number Atrial fibrillation and nodal tachycardia were noted in two and in one patient respectively Ventricular t achy card i a was observed in four patients, two of whom had ventricular fibrillation on admission.

FIGURE 4: Frequent premature ventricular beats In the last ECG strip, ventricular fibrillation followed three successive premature beats (continuous recording).

FIGURE 1: Avionics’ monitoring system The unit, on the right side of the picture, represents the

520

INTRODUCTION

*From the Department of Medicine, University

of Texas Southwestern Medical School.

**Associate Professor of Medicine.

f Present address - intern in Medicine at

Part of this work was presented at the Texas

November, l965.’

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ventricular tachycardia and fibrillation should be managed ing to ESC guidelines 7 In patients with cardiac arrest and who are unresponsive to conventional cardiopulmonary resuscitation,

accord-it is reasonable to use mechanical chest compression devices and emergency cardiopulmonary bypass support is reported to be fea- sible In hemodynamically unstable patients with refractory inces- sant VT, percutaneous left ventricular assist devices (LVADs) may

be appropriate (see below) Following intervention, the incidence

of arrhythmias ranges from 6% to 28% for new-onset AF, 7-13%

Catheter ablation of sustained VA in ACS

Figure 4 Catheter ablation of VA in patients with ACS

AAD: antiarrhythmic drug; ACS: acute coronary syndrome;

ES: electrical storm; PVC: premature ventricular complex;

VA: ventricular arrhythmia; VT: ventricular tachycardia

Table 1 Occurrence of arrhythmias in STEMI patients during and

VF: ventricular fibrillation; VT: ventricular tachycardia

and 3-6% for VF according to retrospective registry data or spective recordings from cardiac monitors implanted soon during

pro-an acute MI 73

The occurrence of AF is frequently associated with severe LV damage and heart failure Episodes may last from minutes to hours and are often repetitive The arrhythmia is most often well toler- ated and no specific treatment is required, other than anticoagulation In some instances, the fast ventricular rate contributes to heart failure, requiring prompt treatment using direct current cardioversion (DCCV) with further management as indicated below Several studies have suggested that development of AF in the setting of acute MI is an independent predictor of all-cause mortality, irrespective of the treatment given 74,75 Atrial fibrillation not only increases the risk for ischaemic stroke during hospitalization but also during follow-up, and this includes patients with paroxysmal AF that has reverted to sinus rhythm at the time of discharge Accordingly, patients with AF and risk factors for thromboem- bolism should be adequately treated with oral anticoagulation Because AF will generally require anticoagulation, when choosing

a stent in these patients, the benefits of drug-eluting stents on nosis should be weighed carefully against the substantial bleeding risks that are associated with the prolonged combination of triple antithrombotic therapy (see below) Other supraventricular tachycardias are uncommon and are usually self-limiting.

reste-Ventricular premature beats are almost universal on the first day of the acute phase and more complex arrhythmias (multiform complexes, short runs, or the R-on-T phenomenon) are common Their value

as predictors of VF is questionable No specific therapy is required The long-term prognostic significance of early (<48 h) VF or sustained VT in patients with acute MI is still controversial.

In the APEX-AMI trial, VT/VF occurred in ~6% of patients with STEMI presenting for primary PCI 15 Two-thirds of these events occurred before the end of cardiac catheterization (defined as early events) and 90% within 48 h Ventricular tachycardia/VF was not benign and was associated with substantially increased morbidity and mortality Some of this association was related to older age, greater prevalence of comorbid conditions, and adverse presenting and post-cardiac catheterization features (ST resolution and TIMI flow) as shown by the attenuation of the risk with adjustment of these factors in a multivariate model However, even after accounting for these variables, any VT/VF remained associated with a more than 3-fold higher risk of 90-day mortality in patients undergoing primary PCI The prognostic significance of late VT/VF appeared

to be greater than early VT/VF with more than 5- and 2-fold higher risks of 90-day mortality, respectively Thus, these data support the prognostic importance of (any, early, or late) VT/VF as an independent and incremental risk marker, although this does not prove

a cause-andeffect relationship However, sustained VT/VF after primary PCI in the HORIZONS-AMI trial was not significantly associated with 3-year mortality or major adverse clinical events 76

Clinical management of sustained VT and VF after primary PCI is according to ESC guidelines 7

Tỷ lệ mắc các rối loạn nhịp thất trong ACS

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Tỷ lệ mắc các rối loạn nhịp thất theo vùng NMCT

International Journal of Contemporary Medical Research Volume 3 | Issue 5 | May 2016 | ICV: 50.43 |

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Cardiac arrhythmias in acute coronary syndromes

with a relevant stenosis in the non-culprit vessel 14 These patients remain at risk for recurrent ischaemic events even after the acute revascularization procedure and seem to be at increased risk for sustained VA 14 A careful review of the coronary anatomy can identify these patients Emerging data suggest that early completion of revascularization may be beneficial, but further data are needed 15

ARRHYTHMOGENIC SUBSTRATE PRIOR TO THE INDEX EVENT Most patients survive their first ACS Owing to progression of arte- riosclerosis, a second acute event will often occur despite maxi- mal preventive therapy Patients who suffer from an acute coronary event with pre-existing reduced LV function and myocardial scars are at risk for sustained VA in the acute and sub-acute phase of

Figure 1 Scheme of drivers for arrhythmias in acute coronary syndromes.Apre-existing substrate for ventricular arrhythmias, either

secondary to an old myocardial infarction, due to a cardiomyopathy, or secondary to a genetic predisposition to ventricular arrhythmias, interacts with acute ischaemia, autonomic tone, and acute left ventricular strain to create triggered activity and ventricular arrhythmias 4

ARVC: arrhythmogenic right ventricular cardiomyopathy; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy;

VF: ventricular fibrillation; VT: ventricular tachycardia; WPW: Wolf-Parkinson-White syndrome (Adapted from Heart, Kirchhof P, Breithardt

G, Eckardt L Primary prevention of sudden cardiac death, 92, 1873-8, Copyright 2006, with permission from BMJ Publishing Group Ltd and from J Cardiovasc Pathol, 19, Basso C, Rizzo S, Thiene G The metamorphosis of myocardial infarction following coronary recanalization, 22-8, Copyright 2010, with permission from Elsevier).

Sinh lý bệnh

của rối loạn

nhịp thất trong

NMCT cấp

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These variables included the same covariates as in the 30-day

mortality model listed above, as well as sex, smoking status, diabetes

mellitus, and prior heart failure.

In both the 30-day and 1-year models, we also adjusted for randomized treatment strategy (early versus delayed provisional

eptifibatide) and prerandomization medications known to influence

survival (angiotensin-converting enzyme inhibitor/angiotensin

re-ceptor blockade, statin, and !-blockers) For the 30-day mortality

model, because we used a 48-hour landmark, we also could adjust for

revascularization (percutaneous or surgical) within 48 hours of

randomization To adjust for revascularization in the 1-year model,

we used percutaneous coronary intervention or surgical

revascular-ization as a time-dependent covariate Finally, we also adjusted for

left ventricular ejection fraction using a categorical variable ("0.50,

0.30 – 0.49, !0.30) as recorded on the case report form Interaction

terms were included for the left ventricular ejection fraction category

and sustained VT/VF P for the interaction tests was based on the use

of ejection fraction "50% as a reference category in the models.

In all analyses, a 2-tailed value of P!0.05 was considered

statistically significant Odds ratios with 95% confidence intervals

(CIs) described the association of sustained VT/VF with 30-day

mortality in both unadjusted and adjusted models Hazard ratios with

95% CIs described the association of sustained VT/VF with 1-year

mortality No adjustments were made for multiple comparisons All

statistical analyses were performed with SAS statistical software

version 9.1 (Cary, NC).

Results

Incidence of Sustained Ventricular Arrhythmias

Among the 9211 patients analyzed, 141 (1.5%) had sustained

VT/VF after randomization Seventy patients (0.8%) had

sustained VT "30 seconds or requiring intervention for

hemodynamic distress, and 84 (0.9%) had VF Figure 1

shows the cumulative incidence of all sustained VT/VF

events The median time to the development of sustained

VT/VF was 5 days (25th and 75th percentiles, 4 and 6 days).

The frequency of sustained VT/VF #48 hours after

random-ization (n#55 of 9211, 0.6%) was similar to that "48 hours

after randomization (n#86 of 9211, 0.9%).

Baseline Characteristics

Baseline characteristics of the full study population (n#9211)

according to the occurrence of sustained VT/VF are shown in

Table 1 More patients with sustained VT/VF had a Killip class higher than I, an elevated troponin at baseline, and prior angina The TIMI risk profile and frequency of prior MI were similar between groups Patients with sustained VT/VF less often received upfront thienopyridine therapy and had lower estimated creatinine clearance at baseline Time from hospitalization to randomization and time from randomization to catheterization were similar in those with and without sustained VT/VF Patients with sustained VT/VF were more likely to have severe left ventricular dysfunction (22.4% versus 4.7% with ejection fraction !0.30), although 40% of all patients with sustained VT/VF had an ejection fraction

"0.50.

In-Hospital Events After Randomization

Of the 6608 patients who underwent revascularization, 1.6% (n#108) had sustained VT/VF The frequency of sustained VT/VF relative to revascularization was as follows: 12% (n#13 of 108) occurred before revascularization, 50% (n#54

of 108) occurred the same day as the revascularization procedure, and 38% (n#41 of 108) occurred after revascularization Among those patients who survived to 30 days, the median time from admission to discharge was 10 days (25th and 75th percentiles, 5 and 14 days) versus 5 days (25th and 75th percentiles, 3 and 8 days) in those with and without sustained VT/VF, respectively.

Predictive Model for Sustained VT/VF

Table 2 shows the results of multivariable modeling for factors associated with the occurrence of sustained VT/VF A calibration curve for the VT/VF model is shown in Figure 2 There is reasonably close agreement between predicted and actual event rates However, there is some underestimation and overestimation within the range of the observed data Eight characteristics were identified as independently associated with sustained VT/VF Increasing systolic blood pres- sure and estimated creatinine clearance were associated with

a lower risk of sustained VT/VF, whereas higher white blood cell count, heart rate, and body weight were associated with

Figure 1 Cumulative incidence of

sus-tained ventricular tachycardia/ventricular fibrillation (VT/VFib) after randomization while accounting for the competing risk of death 18

Rối loạn nhịp thất sau NSTEMI

EARLY ACS trial

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Các YTNC của rối loạn nhịp thất bền bỉ trong NMCT cấp

•  Sốc tim hay tổn thương cấp động mạch vành lớn (VD: thân chung ĐMV trái)

•  Chậm trễ trong tái thông ĐMV

•  Tái thông không được hay không hoàn toàn ĐMV thủ phạm do vấn đề kỹ thuật hay giải phẫu khó khăn

•  Có suy chức năng thất trái hay sẹo cơ tim do NMCT cũ hay ST do bệnh cơ tim trước đó

•  Bệnh cơ tim rối loạn nhịp do di truyền

Willich and Goette Int J Crit Care Emerg Med 2015, 1:2

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Rối loạn nhịp thất sau NMCT cấp

•  RL nhịp thất hay gặp hơn trong STEMI so với NSTEMI (gấp 4 lần)

•  STEMI: 90% xảy ra trong 48 giờ đầu

•  NSTEMI: 60% xảy ra sau 48 giờ

•  Tỷ lệ xuất hiện: NNT không bền bỉ (13%), NNT bền bỉ (3%) và rung thất (3%)

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Tiên lượng của NMCT có rối loạn nhịp thất

•  Tổng hợp 4 nghiên cứu lớn: GUSTO, PURSUIT, PARAGON A, PARAGON B

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ventricular arrhythmias with higher mortality, suggesting that these arrhythmias may lead to increased risk.

Predicting the occurrence of these ventricular arrhythmias

is of vast importance To our knowledge, our study is the first

to identify predictors of such ventricular arrhythmias in this population Significant independent predictors of VF were history of hypertension, history of chronic obstructive pul- monary disease, prior myocardial infarction, and ST-segment changes at presentation Except for hypertension, these clinical variables also were significant predictors of VT It is not surprising that ST-segment changes at presentation strongly predict ventricular arrhythmias, given that these changes may correlate with a greater degree of ischemia It is unclear why chronic obstructive lung disease is a strong predictor of VF and VT, but chronic hypoxia or acidosis combined with ischemia could predispose patients to ventricular arrhythmias.

Thus, patients who have these clinical characteristics may benefit from earlier, more aggressive interventions.

Limitations

The main limitation of this study is that because detailed information about the postdischarge procedures and medications was unavailable, we could not explore their relationships with outcomes.

Implications

Mortality of patients with NSTE-ACS and sustained ventricular arrhythmias is significantly higher than that of NSTE-ACS patients without these arrhythmias Therefore, every effort should be made to identify therapies that would most improve the outcome of these patients This would best be accomplished

by randomized clinical trials of the available antiarrhythmic therapies, including implantable cardioverter-defibrillators.

Acknowledgments

The studies described herein were sponsored by Boehringer heim, Indianapolis, Ind; Ciba Geigy (now Novartis), Summit, NJ; Guidant Corporation, Redwood City, Calif; COR Therapeutics, Inc, South San Francisco, Calif; Schering-Plough Research Institute, Kenilworth, NJ; and F Hoffman La-Roche, Ltd, Basel, Switzerland.

Mann-References

1 Newby KH, Thompson T, Stebbins A, et al Sustained ventricular rhythmias in patients receiving thrombolytic therapy: incidence and

ar-outcomes Circulation 1998;98:2567–2573.

2 The GUSTO-IIb Investigators A comparison of recombinant hirudin with

heparin for the treatment of acute coronary syndromes N Engl J Med.

1996;335:775–782.

3 The PURSUIT Trial Investigators Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients with acute coronary syndromes.

N Engl J Med 1998;339:436 – 443.

4 The PARAGON Investigators International, randomized, controlled trial

of lamifiban (a glycoprotein IIb/IIIa Inhibitor), heparin, or both in

unstable angina Circulation 1998;97:2386 –2395.

5 The PARAGON B investigators Patient-specific dosing of IIb/IIIa tagonists during acute coronary syndromes: rationale and design of the

an-PARAGON B study Am Heart J 2000;139:563–566.

6 Cox DR Regression models and life-tables J R Stat Soc B 1972;34:

8 Gregoratos G, Cheitlin MD, Freedman RA, et al ACC/AHA guidelines

for implantation of cardiac pacemakers and antiarrhythmia devices J Am

Coll Cardiol 1998;31:1175–1209.

9 First International Study of Infarct Survival (ISIS) Collaborative Group Randomised trial of intravenous atenolol among 16,027 cases of sus-

pected acute myocardial infarction: ISIS-1 Lancet 1986;2:57– 66.

10 The BHAT Study Group A randomized trial of propranolol in patients

with acute myocardial infarction: I Mortality results JAMA 1982;247:

1707–1714.

TABLE 4 Mortality by Ventricular Arrhythmia

VT Only vs Neither VF Only vs Neither VF and VT vs Neither

30-Day mortality 11 (8–15) 8 (5–10) 26 (21–33) 23 (18–30) 68 (52–89) 85 (64–114) 6-Month mortality 7 (6–10) 5 (4–7) 15 (12–18) 15 (12–18) 38 (29–49) 37 (29–49) Data are shown as HR (95% CI).

Kaplan-Meier curves of mortality by ventricular arrhythmia.

Sustained Ventricular Arrhythmias Among Patients With Acute Coronary Syndromes With No ST-Segment Elevation – Al Khatib et

al – Circulation July16,2002

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•  Rung thất sớm trong vòng 48 giờ sau NMCT: tử vong tăng 5 lần so với NMCT không có rung thất

•  Trên những bệnh nhân NMCT sau can thiệp ĐMV, nếu

có NNT/RT: tỷ lệ tử vong tăng 4 lần, biến cố tim mạch tăng 3 lần, thời gian nằm viện tăng 50%

Sustained Ventricular Arrhythmias Among Patients With Acute Coronary Syndromes With No ST-Segment Elevation – Al Khatib et al – Circulation July16,2002

The American Journal of Medicine, Vol 121, No 9, September 2008

Trang 14

more often discharged with amiodarone (13.8 vs 7.4%, P ¼ 0.027)

and ACE-inhibitor/ARB (81.2 vs 70.4%, P ¼ 0.031) than patients

without VF Left-ventricular ejection fraction was lower at discharge

among VF patients than non-VF patients (46.6 vs 52.0%, P , 0.001).

The rate of ICD implantation during in-hospital course was low (0.3%

in the overall population), but higher in the VF group (3.4 vs 0.2%, P ,

0.001) After 3 years of follow-up (available in 97.8% of patients),

pharmacological therapies no longer differed between the two

groups, including antiarrhythmic medications, particularly

amiodar-one (P ¼ 0.22) An additional 35 patients received an ICD during

the first 3 years of follow-up, all of these in the non-VF group,

giving an overall ICD implantation rate of 1.2%, not significantly

differ-ent between VF (3.4%) and non-VF (1.2%) groups.

Among 3463 survivors at hospital discharge, 1024 died during a

mean follow-up of 52 + 2 months, giving an overall survival rate at

5 years of 74.4% (95% CI 72.8–76.0%) Survival rates were 81.3%

(95% CI 73.1–89.5%) in the VF group compared with 74.2% (95%

CI 72.6–75.8%) in the non-VF group (Figure 2 ) In multivariate lysis, after adjustment for other prognostic factors, occurrence of

ana-VF during the acute phase of MI was not associated with any increase

in mortality at 5 years (HR for mortality 0.78, 95% CI 0.38–1.58, P ¼ 0.21), in both STEMI and non-STEMI patients When considering timing of VF, neither early VF (OR 0.5, 95% CI 0.2–1.1, P ¼ 0.09) nor late VF (OR 1.9, 95% CI 0.6–5.9, P ¼ 0.30) was associated significantly with long-term mortality When we consider the additional 75 cases of VT to the VF group, in multivariate analysis, after adjustment for other prognostic factors, occurrence of sustained ventricular arrhythmias (VT and VF considered together) during the acute phase of MI was not associated with significant increase in mortality

No VF (178/3554)

P-value

,0.001 Sudden cardiac death, n (%) 11 (37.9) 52 (29.2)

No VF (n 5 3376)

P-value

Beta-blockers, n (%) 72 (84.7) 2582 (77.9) 0.134 Aspirin, n (%) 81 (93.1) 3089 (92.2) 0.745 Clopidogrel, n (%) 72 (82.8) 2707 (80.9) 0.667 Statins, n (%) 73 (84.9) 2788 (83.9) 0.802 ACE-inhibitor or

ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; VF, ventricular fibrillation.

60

50 40 30

60 50 40 30 20 10

0 Patients without VF Patients with VF No VF Early VF Late VF

Figure 1 In-hospital mortality according to occurrence of ventricular fibrillation.

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The American Journal of Medicine 2008 121, 797-804DOI: (10.1016/j.amjmed.2008.04.024)

Các yếu tố dự báo NNT bền bỉ sau NMCT cấp

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Tử vong và RLNT tăng theo số yếu tố nguy cơ

The American Journal of Medicine 2008 121, 797-804DOI: (10.1016/j.amjmed.2008.04.024)

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Tử vong tăng ở nhóm can thiệp thất bại

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Làm thế nào phòng ngừa và điều trị

trong NMCT cấp ???

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PRACTICE GUIDELINE

2012 ACCF/AHA/HRS Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for

Device-Based Therapy of Cardiac Rhythm Abnormalities

A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society

Developed in Collaboration With the American Association for Thoracic Surgery

and Society of Thoracic Surgeons

2008 WRITING COMMITTEE MEMBERS

Andrew E Epstein, MD, FACC, FAHA, FHRS, Chair; John P DiMarco, MD, PH D, FACC, FHRS;

Kenneth A Ellenbogen MD, FACC, FAHA, FHRS; N.A Mark Estes III, MD, FACC, FAHA, FHRS;

Roger A Freedman, MD, FACC, FHRS; Leonard S Gettes, MD, FACC, FAHA;

A Marc Gillinov, MD, FACC, FAHA; Gabriel Gregoratos, MD, FACC, FAHA;

Stephen C Hammill, MD, FACC, FHRS; David L Hayes, MD, FACC, FAHA, FHRS;

Mark A Hlatky, MD, FACC, FAHA; L Kristin Newby, MD, FACC, FAHA;

Richard L Page, MD, FACC, FAHA, FHRS; Mark H Schoenfeld, MD, FACC, FAHA, FHRS;

Michael J Silka, MD, FACC; Lynne Warner Stevenson, MD, FACC#; Michael O Sweeney, MD, FACC

Developed in Collaboration With the American Association for Thoracic Surgery,

Heart Failure Society of America, and Society of Thoracic Surgeons

2012 WRITING GROUP MEMBERS*

Cynthia M Tracy, MD, FACC, FAHA, Chair; Andrew E Epstein, MD, FACC, FAHA, FHRS, Vice Chair*;

Dawood Darbar, MD, FACC, FHRS†; John P DiMarco, MD, P H D, FACC, FHRS*‡;

Sandra B Dunbar, RN, DSN, FAAN, FAHA†; N.A Mark Estes III, MD, FACC, FAHA, FHRS*§;

T Bruce Ferguson, J R , MD, FACC, FAHA*!¶; Stephen C Hammill, MD, FACC, FHRS‡;

Pamela E Karasik, MD, FACC, FHRS†; Mark S Link, MD, FACC, FHRS*†;

Joseph E Marine, MD, FACC, FHRS†; Mark H Schoenfeld, MD, FACC, FAHA, FHRS*†;

Amit J Shanker, MD, FACC, FHRS‡; Michael J Silka, MD, FACC†; Lynne Warner Stevenson, MD, FACC*#;

William G Stevenson, MD, FACC, FAHA, FHRS***; Paul D Varosy, MD, FACC, FHRS†

*The 2012 writing group members were required to recuse themselves from voting on sections to which their specific relationships with industry and other

#Heart Failure Society of America Representative **ACCF/AHA Task Force on Practice Guidelines Liaison.

This document was approved by the American College of Cardiology Foundation Board of Trustees, the American Heart Association Science Advisory and Coordinating Committee, and the Heart Rhythm Society Board of Trustees in May 2012.

The American College of Cardiology Foundation requests that this document be cited as follows: Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and

the Heart Rhythm Society J Am Coll Cardiol 2013;61:e6–75.

This article is copublished in Circulation.

Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the

Journal of the American College of Cardiology Vol 61, No 3, 2013

and the Heart Rhythm Society http://dx.doi.org/10.1016/j.jacc.2012.11.007ISSN 0735-1097/$36.00Published by Elsevier Inc.

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Phòng ngừa và điều trị đột tử trong hội chứng

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Induction of polymorphic VT or VF, especially with aggressive

stimulation techniques, is not specific In CAD, the diagnostic yield

may reach 50%.

Figure 1 illustrates the proposed diagnostic workflow for patients

who survived an aborted cardiac arrest, while the management

of cardiac arrest in the setting of specific conditions is described

in sections 5–12 Web Table 3 presents the nomenclature adopted

when referring to VAs across this document 122 Investigations that

may reveal disease-specific findings are detailed in Web Table 4.

4 Therapies for ventricular arrhythmias

4.1 Treatment of underlying heart disease

A fundamental aspect of the successful management of VA and the prevention of SCD is effective management of underlying diseases and co-morbidities Acute worsening and progressive deterioration

of these conditions must be avoided Co-morbidities that may

Clinical History

• Angina pectoris or shortness of breath

• Family history of premature SCD (age <40 years) or ealy-onset heart disease

• ECG during tachycardia

Other transient cause e.g.

• Drugs

• Electrolytes

• Chest trauma

Evaluate for cardiovascular diseases

Reverse transient cause

Acute ischemia

(STEMI, NSTEMI)

Secondary prevention for SCD (ACEi, beta-blockers, statin, antiplatelets)

Re-evaluate LVEF 6–10 weeks after event

Consider ICD according to secondary prevention

Urgent angiogram and revascularisation

• Treatment of underlying heart disease (e.g valve repair, medication)

• Assess risk for SCD

on cause of VT/VF

ECG Echocardiogram History and Family history a

Structural heart disease and congenital heart diseases

suspected (e.g Stable CAD, sarcoidosis, aortic valve disease, DCM)

Inherited arrhythmogenic disease or cardiomyopathy

suspected

No detectable heart disease

Sudden death victims

• Autopsy in collaboration with pathologists

• Obtain blood and tissue samples

• Molecular autopsy after autopsy

• Offer family councelling and support

• Refer family for cardiology / SCD workup

Further patient assessment, e.g b

• Stress test, Holter 48 hours,

• Consider coronary angiogram

• Refer patients to experienced centers for risk evaluation, catheter ablation, drugs and ICD

• Drug challenges, EPS

• CMR, CT, myocardial biopsy

• Signal averaged ECG, TOE based on suspected disease

ACEi = angiotensin-converting enzyme inhibitors; CAD = coronary artery disease; CMR = cardiac magnetic resonance; CT = computed tomography; DCM = dilated cardiomyopathy;

ECG = electrocardiogram; EPS = electrophysiological study; GL = guidelines; ICD = implantable cardioverter

LVEF = left ventricular ejection fraction; NSTEMI = non-ST-segment elevation myocardial infarction; SCD = sudden cardiac death;

STEMI = ST-segment elevation myocardial infarction; TOE = transoesophageal echocardiography; VF = ventricular

VT = ventricular tachycardia.

a Clinical history of chest pain, dyspnoea, and symptoms associated with certain cardiac conditions and family tree

b The need for further tests and evaluations will be guided by the initial assessment and by suspected cardiovascular diseases.

Figure 1 Diagnostic workup in patients presenting with sustained ventricular tachycardia or ventricular fibrillation.

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Cardiac arrhythmias in acute coronary syndromes

patients with advanced heart failure 32 It belongs therefore to the

few AADs that are considered to have no or little effect on

long-term prognosis when given to patients with severe structural heart

disease and/or extensive MI In the context of ACS, amiodarone

therapy – compared with lidocaine – retrospectively has shown an

increased short- and long-term mortality 20 On the other hand, in the

setting of out-of-hospital cardiac arrest, amiodarone was associated

with better survival to admission rate as compared with lidocaine in

patients with refractory to shock therapy VF 33 Amiodarone should

be considered for the suppression (intravenous or oral) and

preven-tion (oral) of recurrent arrhythmias along with beta-blockers.

Flecainide, propafenone, and ajmaline exert their

antiarrhyth-mic potential by significant slowing of conduction In the setting

of ACS, these effects may result in aggravation rather than

termi-nation of VT/VF The antiarrhythmic potential of these AADs for

the suppression and termination of VA has been mainly studied

until the 1990s 34-37 However, in the setting of ACS, these drugs

may cause an aggravation of VT/VF After the publication of the

CAST trial that has shown an increased mortality in patients after

MI treated with encainide, flecainide, or moricizine as compared

with placebo, further research to class IAAD and VA has largely

been abandoned 26 Thus, these drugs should not be used in ACS.

Dofetilide and azimilide are class III AADs that prolong

car-diac repolarization and refractory period with proven efficacy on

the suppression of VA 38-40 The treatment with azimilide did not

affect the mortality of patients with a recent MI and an LV ejection

fraction of 15% to 35% 41 Only few data exist on the use of

drone-darone for the treatment of VA; however, an increased mortality

has been reported in patients with AF and heart failure treated

with dronedarone 42 All class III AADs increase the QT interval

with a risk for torsade de pointes tachycardias However, none of

these drugs had been specifically investigated for the treatment

of VA related to ACS and can thus not be recommended for this

indication.

Ranolazine is a piperazine derivative with a chemical structure

similar to that of lidocaine The MERLIN-TIMI 36 study

rand-omized 6560 patients with ACS to ranolazine or placebo 43 Although

there was no significant difference in the combined primary

end-point of cardiovascular death, MI, or recurrent ischaemia, the

inci-dence of non-sustained VT (<30 s) was significantly reduced by

ranolazine compared with placebo 43,44 The role of ranolazine as an

AAD is nevertheless still investigational 45

Recommendations for antiarrhythmic therapy in patients with

acute coronary syndrome and ventricular tachyarrhythmia

For patients with acute coronary syndrome (ACS) without

ventricu-lar arrhythmias, prophylactic antiarrhythmic drug treatment should

not be administered.

– If life-threatening ventricular arrhythmias related to ACS occur

despite optimal revascularization, early treatment with

beta-blockers, balancing electrolytes, and sedation to reduce

sym-pathetic drive and/or overdrive stimulation, repetitive electrical

cardioversion/defibrillation should be considered first.

Recurrent VT/VF and Electrical Storm in ACS

Cardioversion/defibrillation

Overdrive pacing

Attempt complete revascularization

Treat ischaemia Correct electrolyte imbalance

β-blocker therapy Deep sedation

Recurrent VT/VF Amiodarone Lidocaine Consider catheter ablation

Electrical Storm Amiodarone Consider ICD reprogramming Consider catheter ablation Consider LVAD implantation

Figure 2 Treatment recommendations for recurrent VT/VF and

electrical storm in ACS ACS: acute coronary syndrome; ICD:

implantable cardioverter-defibrillator; LVAD: left ventricular assist device; VF: ventricular fibrillation; VT: ventricular tachycardia

– If antiarrhythmic drug therapy is necessary on top of these measures for the acute treatment of recurrent ventricular arrhythmias related to ACS after failure or non-availability

of other treatment capabilities, administration of intravenous amiodarone is reasonable, followed by intravenous lidocaine,

if necessary (Figure 2).

– When experience is available, early catheter ablation should

be considered when other treatments fail (see below).

– Ventricular tachyarrhythmia in the first minutes after cessful reperfusion therapy can be transient without need for treatment, known as reperfusion arrhythmias.

suc-– If frequent premature ventricular complexes and tained ventricular tachycardia continue despite successful reperfusion therapy under sufficient beta-blocker therapy, they should only be treated if hemodynamically important

non-sus-This treatment should follow the same principles as the ment of sustained VA.

treat-How to manage electrical storm and inappropriate implantable cardioverter- defibrillator shocks in patients with acute coronary syndrome

In patients with ACS, electrical storm and inappropriate ble cardioverter-defibrillator (ICD) shocks are associated with poor prognosis 46-49

implanta-Electrical storm is defined as the three or more episodes of VT

or VF in any 24-hour period 46,50 It results from interplay between pre-existing vulnerable substrate and acute triggers It is a rare but

Phác đồ điều trị rối loạn nhịp thất trong ACS

EuroIntervention 2014;10-online publish-ahead-of-print August 2014

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