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Ischemic Heart Disease

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Presentation on theme: "Ischemic Heart Disease"— Presentation transcript:

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Case 6 - Woman with Ischemic Heart Disease Admitted due to Chest Pain and Shock

Rafael amorim belo nunes.

Instituto do Coração do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (InCor-HC-FMUSP), São Paulo, SP - Brazil

Hilda Sara Montero Ramirez

Vera demarchi aiello.

A 67-year-old woman sought emergency medical care due to prolonged chest pain. In April 2009 the patient had prolonged chest pain and at that time she sought medical care. She was admitted at the hospital and diagnosed with myocardial infarction.

The patient had hypertension, diabetes mellitus, dyslipidemia and was a smoker.

During the patient's evolution, after the myocardial infarction, she was submitted to a coronary angiography in, which disclosed the presence of lesions with 70% obstruction in the right coronary, anterior descending and circumflex arteries. A left ventriculography revealed apical akinesia with signs of intracavitary thrombus in that region.

The echocardiogram (May 2009) disclosed ventricular dysfunction accentuated by diffuse hypokinesis, with a 28% left ventricular ejection fraction. Clinical and drug treatment was recommended to the patient.

The patient's evolution was asymptomatic until October 2009, when she had a cerebrovascular accident, with motor sequela.

On December 30, 2009, the patient had an episode of severe chest pain that lasted for one hour and she sought medical care.

At the physical examination, the heart rate (HR) was 100 beats per minute, blood pressure was 100/60 mmHg. Pulmonary assessment was normal. The heart examination disclosed a ++/ 6+ systolic murmur in the mitral area. The remainder of the physical examination was normal. The electrocardiogram (1h 19 min; Dec 30, 2009) showed sinus rhythm, HR of 103 bpm, PR interval of 122 ms, QRS duration of 159 ms, QT interval of 367 ms, and corrected QT of 480 ms.

There was left atrial overload, low voltage of the QRS complex in the frontal plane, probable inferior electrically inactive area, and left bundle branch block ( Figure 1 ). Chest x-ray disclosed the presence of a large pleural effusion in the right hemithorax.

Electrocardiogram - Sinus rhythm, low voltage of the QRS complex in the frontal plane, electrically inactive area in the inferior wall and left bundle branch block.

The laboratory tests showed hemoglobin 13 g/dL, hematocrit 40%, MCV 91 fL, leukocytes 12,400/mm 3 (66% neutrophils, 1% eosinophils, 1% basophils, 19% lymphocytes and 13% monocytes), 421,000/mm 3 , total cholesterol 228 mg/dL, HDL-cholesterol 35 mg / dL, LDL-cholesterol 162 mg/dL, triglycerides 157 mg/dL, CK-MB mass 5.63 ng / mL, Troponin I 0.21 ng/mL, urea 33 mg/dL, creatinine 0.66 mg/dL, sodium 137 mEq/L, and potassium 3.4 mEq/L. Venous blood gasometry showed pH 7.46, pCO 2 39.3 mmHg, pO 2 36.3 mmHg, O 2 saturation 62.7%, bicarbonate 27.7 mEq/L and base excess 4.1 mEq/L.

Approximately two hours after hospital admission, she had seizures and cardiac arrest with pulseless electrical activity, reversed in 5 min.

The electrocardiogram after the cardiac arrest (4:18 am; Dec 30, 2009) showed a HR of 64 bpm, absence of P waves, and left bundle branch block. The QRS complex alteration, in relation to the previous tracing, was a positive QRS complex in the V6 lead ( Figure 2 ).

Electrocardiogram - Sinus rhythm, left bundle branch block and positive T waves on an also positive derivative of the QRS complex.

She had a new cardiac arrest 20 min later, which was also reversed. After half an hour, a new episode of cardiac arrest occurred, which was irreversible, and the patient died (5:45 am; Dec 30, 2009).

Clinical aspects

This patient is a 67-year-old woman with cardiovascular risk factors and ischemic cardiomyopathy, with severe left ventricular systolic dysfunction. Cardiac catheterization disclosed multivessel coronary disease and apical akinesis with an intracavitary thrombus. During outpatient follow-up, clinical treatment was chosen, possibly influenced by the patient's clinical status, as well as the characteristics of the coronary anatomy.

The indication of surgical treatment with myocardial revascularization in patients with coronary heart disease with heart failure and severe left ventricular systolic dysfunction is still debatable, but recent data from the STICH study suggest a long-term survival benefit in patients undergoing myocardial revascularization. 1

During follow-up in October 2009, the patient had a clinical picture suggestive of a cerebrovascular accident that may have been of atherothrombotic origin due to the multiple cardiovascular risk factors or of cardioembolic origin, associated with intracavitary thrombi.

In December 2009 the patient was admitted to the emergency room with acute chest pain. She had mild tachycardia and borderline systolic blood pressure of 100 mmHg. The electrocardiogram showed sinus tachycardia, left atrial overload and left bundle branch block.

In patients with acute chest pain and electrocardiogram with acute or undetermined left bundle branch block, the possibility of acute myocardial infarction should be considered, especially in case of hemodynamic instability. Criteria such as those proposed by Sgarbossa et al., 2 and Smith et al., 3 modified by other authors can contribute to the diagnostic accuracy improvement in this context. 2 , 3 However, one should consider that the occurrence of left bundle branch block is more commonly a marker of previous structural heart disease.

The patient had a cardiorespiratory arrest with pulseless electrical activity (PEA) within a short time after hospital admission. In cases of acute myocardial infarction, PEA can occur in patients with severe ventricular dysfunction and cardiogenic shock and/or mechanical complications such as rupture of the left ventricular free wall with cardiac tamponade, papillary muscle rupture and / or severe dysfunction and acute interventricular septal defect.

Other conditions should be considered in patients with acute chest pain who present with rapid clinical deterioration such as aortic dissection and pulmonary thromboembolism. The chest x-ray showed a massive pleural effusion in the right hemithorax, although this finding was not readily apparent at the physical examination. In this patient, pleural effusion may be due to chronic heart failure decompensation but may also be associated with other conditions, such as rheumatologic diseases, tuberculosis or pleural carcinomatosis due to neoplasias. The last two conditions mentioned here are not uncommon in patients with chronic heart diseases.

Additionally, massive pleural effusions may coexist, in some conditions, with pericardial involvement and consequent cardiac tamponade. 4 Pleural effusion may also be present in patients with acute aortopathies, such as dissection of the aorta and aortic ulcer with associated rupture, but usually the most frequent effusion is located in the left pleural space as a consequence of the aortic anatomy. (Dr. Hilda Sara Montero Ramirez)

Main hypothesis: Acute myocardial infarction complicated by cardiogenic shock. ( Dr. Hilda Sara Montero Ramirez )

Differential diagnoses: Cardiac tamponade, Pulmonary thromboembolism and Dissection of the aorta. ( Dr. Hilda Sara Montero Ramirez )

The heart weighed 422 g and showed increased volume, with cross-sections (short axis of the ventricles) disclosing a healed transmural myocardial infarction in the left ventricular anterior and septal walls. There was wall thinning and fibrosis, with antero-apical aneurysm and thrombus at the apex ( Figure 3 ). Signs of a previous systemic thromboembolism, with previous renal and cerebral infarctions were also found, with the latter being a cavitated infarction affecting the temporal and occipital regions of the left cerebral hemisphere.

Cross-sections of the heart at the level of the ventricles (short axis) showing previous transmural infarctions in the anterior and septal walls (arrows). These same places show thinning of the wall and, localized slight dilatation (aneurysm). There is also a cavitary thrombus in the ventricular apex (asterisk).

The aorta and coronary arteries showed marked atherosclerotic involvement, with ulcerated plaques in the aorta and obstructions > 70% in the initial and middle thirds of the anterior interventricular branch of the left coronary artery and between 50 and 70% in the circumflex branch of the same artery and in the right coronary artery. Signs of congestive heart failure were found in the lungs and liver.

The terminal cause of death was pulmonary thromboembolism on the right, with infarction organization at the pulmonary base ( Figure 4 ). The right pleura showed fibrin deposits and the histological analysis showed acute fibrinous pleuritis ( Figure 5 ). There was also pleural effusion on the right (500mL of citrine-colored fluid) ( Prof. Dr. Vera D. Aiello ).

Right lung cross-section at its long axis showing the presence of thromboembolism in the central branch of the pulmonary artery (arrow). At the base, there are two triangular areas (asterisks) where the parenchyma is homogeneous and reddish in color, corresponding to recent pulmonary infarctions.

Photomicrography of the right pleura showing neutrophilic exudate on the surface (asterisk), characterizing acute pleuritis. Hematoxylin-eosin staining, objective magnification = 10X.

Anatomopathological diagnoses

• - Ischemic heart disease with healed transmural infarctions in the anterior wall and ventricular septum and anteroseptal aneurysm.
• - Apical thrombus in the left ventricle.
• - Systemic and coronary atherosclerosis of moderate to high degree.
• - Previous infarctions in the kidneys and in the temporal and occipital cortex of the left cerebral hemisphere.
• - Pulmonary thromboembolism on the right, with recent pulmonary infarction.
• - Acute fibrinous pleuritis on the right, with pleural effusion (500mL) ( Prof. Dr. Vera D. Aiello )

The patient described herein sought emergency care with chest pain and was known to have ischemic heart disease. The clinical investigation for acute infarction was inconclusive and the patient died less than 24 hours after hospital admission.

Necropsy showed previous infarctions and signs of congestive heart failure. We found no evidence of a recent infarction and attributed the chest pain to the finding of a recent pulmonary thromboembolism on the right, with pulmonary infarction and acute fibrinous pleuritis.

In a study carried out at our institution, which assessed the agreement between clinical diagnoses and necropsy findings, the greatest discrepancy occurred in cases of pulmonary thromboembolism (34.1%). 5 ( Prof. Dr. Vera Demarchi Aiello )

Section Editor: Alfredo José Mansur ( rb.psu.rocni@rusnamja )

Associated Editors: Desidério Favarato ( rb.psu.rocni@otaravaflcd ) Vera Demarchi Aiello ( rb.psu.rocni@arevpna )

ISCHEMIC HEART DISEASE

Aug 22, 2014

580 likes | 1.56k Views

ISCHEMIC HEART DISEASE. I. Chief Complaint. " Doc, the drugs aren't working for my chest pain!”. HPI.

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• frequent angina
• low back pain
• facial asymmetry
• myocardial oxygen demand
• coronary artery bypass operations

Presentation Transcript

ISCHEMIC HEART DISEASE I

Chief Complaint "Doc, the drugs aren't working for my chest pain!”

HPI Jack Palmer is a 72-year-old man with coronary artery disease. He is an avid golfer and prefers to walk the course, but this is becoming progressively more difficult for him due to frequent angina. He has had two coronary artery bypass operations in the past. A coronary angiogram performed 1 month ago revealed significant disease in the RCA proximal to his graft but this was considered high risk for angioplasty. His dose of isosorbidemononitrate was increased at that time from 60 to 120 mg once daily. This had no effect on his angina. He is still using about 30 nitroglycerin tablets a week, and these do relieve his chest pain. He reports that most often the chest discomfort comes on with activity, such as walking up slight inclines on the golf course. The discomfort is located in the center of his chest and rated as a 3–4/10 on average. He reports that the chest discomfort slowly fades as he slows his activity. He also complains of occasional lightheadedness with a pulse around 50 bpm and SBP near 100 mm Hg.

PMH . Acute anterior wall MI with CABG in 1976 . Posterior lateral MI in 1990 and PTCA to the circumflex at that time . Redo CABG in 1998 . Ischemic cardiomyopathy . Heart failure with an ejection fraction of 40% . Dyslipidemia . COPD (mild) . Chronic low back pain . Depression

FH Noncontributory for premature coronary artery disease SH Retired dairy farmer, lives with wife, drinks occasionally, previous smoker—quit in 1998

Meds Carvedilol 6.25 mg twice daily Digoxin 0.25 mg once daily Lisinopril 5 mg once daily Furosemide 40 mg once daily Aspirin 325 mg once daily Isosorbidemononitrate, extended release 120 mg once daily

Meds Diltiazem, extended-release 240 mg once daily St. John's wort 300 mg three times daily Celecoxib 200 mg once daily Simvastatin 40 mg once daily Nitroglycerin 0.4 mg SL PRN

AII NKDA ROS No fever, chills, or night sweats. No recent viral illnesses. No shortness of breath; occasional cough with cold weather. No nausea, vomiting, diarrhea, constipation, melena, or hematochezia. No dysuria or hematuria. No myalgias or arthralgias.

Physical Examination Gen Pleasant, cooperative man in no acute distress VS BP 105/68, P 50, RR 22, T 36.4°C, Ht 5'11″, Wt 93 kg, waist circumference 43 in Skin Intact, no rashes or ulcers

Physical Examination HEENT PERRL; EOMI; oropharynx is clear Neck Supple, no masses; no JVD, lymphadenopathy, or thyromegaly Lungs Bilateral air entry is clear. No wheezes.

Physical Examination CV RRR, S1, S2 normal; no murmurs or gallops; PMI palpated at left fifth ICS, MCL Abd Soft, NT/ND; bowel sounds normoactive Genit/Rect Heme (–) stool

Physical Examination Ext No CCE; pulses 2+ throughout Neuro A & O x 3, CN II–XII intact; speech is fluent; no motor or sensory deficit; no facial asymmetry; tongue midline

MCV 77 m3 MCV 77 m3 Labs Na 137 mEq/L Glu98 mg/dL Hgb 11.8 g/dL K 4.8 mEq/L Cl103mEq/L Hct 35.1% CO2 21 mEq/L Plt187 x 103/mm3 BUN 24 mg/dL WBC7.9 x 103/mm3 SCr1.2 mg/dL MCV 77cm3 MCHC 29 g/dL

MCV 77 m3 MCV 77 m3 Labs Fasting lipid profile: Digoxin serum concentration: 1.8 mg/ml Chol202 mg/dL LDL 125 mg/dL HDL 38 mg/dL Trig 215 mg/dL

ECG Sinus rhythm, first-degree AVB, 50 bpm, old AWMI, no ST–T wave changes noted, QT/QTc 406/431 Assessment A 72-year-old man with poorly controlled angina on multiple medications who is a poor candidate for angioplasty Clinical Pearl The COURAGE trial made major headlines in 2007 by showing that coronary stenting with optimal medical therapy is no better at preventing future coronary events than optimal medical therapy alone in patients with stable coronary disease, potentially saving the US health care system $5 billion a year.14

Questions Problem Identification 1.a. What drug-related problems appear to be present in this patient? • Angina pectoris, poorly controlled on current drug therapy • Dyslipidemia, poorly controlled • More safe drug is recommended instead of Diltiazem because of his mild HF • Unsafe drug is been using Celecoxib due to increase risk of CVD • Safety dosage regimen issues ( digoxin ,aspirin ) • Metabolic syndrome (abdominal obesity, elevated triglyceride and low HDL-C )

1.b. Could any of these problems potentially be caused or exacerbated by his current therapy? • Medical management of angina must take into consideration the patient’s hemodynamic status and left ventricular function. Although CCB and BB are both reasonable antianginal drugs, they are likely the cause of his relatively low heart rate and blood pressure and associated lightheadedness. According to the American Heart Association (AHA)/American College of Cardiology (ACC) guidelines, he should remain on a β-blocker such as carvedilol, if possible, to slow progression of systolic heart failure but diltiazem is a poor choice in a patient with left ventricular dysfunction as it is known to depress myocardial contractility.

• According to a recent statement by the AHA, selective COX-2 inhibitors such as celecoxib increase the risk of myocardial infarction, stroke, heart failure, and hypertension.

Questions Desired Outcome 2. What are the goals of pharmacotherapy for IHD in this case? Short term : Stabilize chest pain and discomfort and reduce and stabilize angina symptoms Prevent ischemia and subsequent infarction Improve exercise tolerance and quality of life Long term : Prevent primary or secondary CV event MI HF Stabilize the pattern of chest pain Decrease overall CV morbidity and mortality

Questions 3.a. Does this patient possess any modifiable risk factors for IHD? Therapeutic Alternatives • He has poorly controlled dyslipidemia. His LDL-C and triglycerides are too high, and his HDL-C is too low. Hypercholesterolemia is a significant cardiovascular risk factor, and risk is directly related to the degree of cholesterol elevation. (target LDL <100 mg/dL; <70 mg/dL in patients with CHD and multiple risk factors is reasonable ) Additional goals include HDL-C greater than 40 mg/dL and triglycerides less than 150 mg/dL. Because his triglycerides are in the range of 200–499 mg/dL, a secondary target is non-HDL cholesterol <130 mg/dL.

• Alcohol ingestion in small to moderate amounts (<40 g/day of pure ethanol) reduces the risk of coronary heart disease; however, consumption of large amounts (>50 g/day) or binge drinking of alcohol is associated with increased mortality from stroke, cancer, vehicular accidents, and cirrhosis •Body mass index is associated with an increased mortality ratio compared with individuals of normal body weight, and the objective for patients with IHD is to maintain or reduce to a normal body weight

• This patient meets the criteria for the definition of metabolic syndrome on the basis of abdominal obesity, elevated triglycerides,and low HDL-C. ATP III1 identified 6 components of the metabolic syndrome that relate to CVD: • 1) Abdominal obesity It presents clinically as increased waist circumference. Waist circumference ≥40 in (102 cm) in men and ≥35 in (88 cm) in women 2) Atherogenic dyslipidemia raised triglycerides and low concentrations of HDL cholesterol. HDL-C <40 mg/dL in men and <50 mg/dL in women Triglycerides ≥150 mg/dL

3) Raised blood pressure ≥130/85 mm Hg 4) Insulin resistance ± glucose intolerance 5) Proinflammatory state recognized clinically by elevations of C-reactive protein (CRP), is commonly present in persons with metabolic syndrome.  6) Prothrombotic statecharacterized by increased plasma plasminogen activator inhibitor (PAI)-1 and fibrinogen, also associates with the metabolic syndrome.

• He is currently taking celecoxib for low back pain, which may put him at risk for cardiovascular events. • All NSAIDs are associated with an increased risk of serious (and potentially fatal ) adverse cardiovascular thrombotic events, including MI and stroke • Risk may be increased with duration of use or pre existing cardiovascular risk factors or disease

3.b. What pharmacotherapeutic options are available for treating this patient's IHD? Discuss the agents in each class with respect to their relative utility in his care. • We use nitroglycerine to relieve acute symptom • Pharmacotherapy to prevent recurrent ischemic symptom -Beta blocker -Calcium channel blocker -Long acting nitrate -Ranolazine • Pharmacotherapy to prevent acute coronary syndromes and death ( vasoprotictive agent ) -Antiplatlet agent -Statin -ACE inhibitors and ARB -Control of risk factors

Nitrate • Nitrate therapy should be first step in managing acute attack for patient with chronic stable angina or for prophylaxis of symptoms.its leading to reductions in preload and afterload reduction of myocardial oxygen demand ,Nitrate –free interval (10-12 hours/day) is recommended to avoid tolerance development . Nitroglycerin (NTG) : Nitroglycerin concentrations are affected by the route of administration, with the highest concentrations usually obtained with intravenous administration, the lowest seen with lower oral doses Isosorbide dinitrate (ISDN): Chewable, oral, and transdermal products are acceptable for the long-term prophylaxis of angina, its given 1 tablet three to four time daily. Isosorbide mononitrate (ISMN):is available in two types of oral formulations: Regular release tablet : initial 5-20 mg BID with the 2 doses given 7 hours apart (eg. 8AM and 3PM )to decrease tolerance development Extended release tablet : initial 30-60 mg given once daily in the morning ;titrate upword as needed maximum daily dose : 240 mg

Calcium channel blockers (CCBs) Calcium channel antagonists have the potential advantage of improving coronary blood flow through coronary artery vasodilation as well as decreasing MVO2. Calcium antagonists may provide better skeletal muscle oxygenation, resulting in decreased fatigue and better exercise tolerance. Patients with conduction abnormalities and moderate to severe LV dysfunction (ejection fraction <35%) should not be treated with verapamil and Diltiazem whereas amlodipine may be safely used in many of these patients. We must consider that this patient has a relatively low heart rate and moderate LV dysfunction. Therefore, use of a negative inotrope such as diltiazem is inadvisable.

B-blockers β-blockers may be preferable because of less-frequent dosing and other properties inherent in β-blockade (e.g., potential cardioprotective effects, antiarrhythmic effects, lack of tolerance, and antihypertensive effects), as well as their antianginal effects and documented protective effects in post- MI patients. Decreased heart rate, decreased contractility, and a slight to moderate decrease in blood pressure with β-adrenergic receptor antagonism reduce MVO2 Carvedilol is a nonselective beta-adrenergic blocking agent with a1 blocking activity This patient has mild COPD but seems to be tolerating his carvedilol well at present.

Ranolazine Ranolazine exerts antianginal and anti-ischemic effects without changing hemodynamic parameters (HR & BP) Ranolazine doesn’t relieve acute angina attack.Has been shown to prolong QT interval We need to avoid grapefruit –contaning product or dose adjusment of ranolazine may be required St John’s wort may decrease the serum concentration of ranolazine With moderate CYP3A inhibitors (e.g., diltiazem, verapamil, erythromycin), the ranolazine dose should be limited to 500 mg twice daily.

Antiplatelet

ACE inhibitors

Questions Optimal Plan 4. Given the patient information provided, construct a complete pharmacotherapeutic plan for optimizing management of his IHD .

1) Stop using Deltiazm and replace it by amlodepine 5mg once daily 2) Stop using of carvidilol and replaced by metoprololtarterateXL 50mg once daily 3) we replace simvastatin by atrovastatines 40mg once daily 4) Decreas the dose of digoxin to .125 once daily 5) Adding of ranalozin 500mg BID6) Reduce the dose of aspirin to 162 mg once daily

7) Initially continue the administration of isosorbidemononitrate 120mg QD,PO then after the patient condition is improved inc.the dose up to 240mg QD,PO8) Discontinue CELECOXIB and start with PARACETAMOL 500mg PRN, PO

Questions Outcome Evaluation 5. When the patient returns to the clinic in 2 weeks for a follow-up visit, how will you evaluate the response to his new antianginal regimen for efficacy and adverse effects?

Efficacy: We need to ask him : about the number and severity of anginal attacks and what provoke his anginal pain .and for how long its remain Does sublingual NTG relieve the pain? Have any attacks occurred at rest which is a sign of unstable angina and would require hospital admission?

Adverse effects: We need to Check vital signs.: heart rate and blood pressure We would ask if he had any of these symptoms dizziness, lightheadedness, headache, and facial flushing. Because we want to give him amlodipine instead of diltiazem we need to check if he had any edema We need to be careful about sign of bleeding

Questions Patient Education • 6. What information will you communicate to the patient about his antianginal regimen to help him experience the greatest benefit and fewest adverse effects?

Nitroglcerin SL • 1) Used at start of angina if the pain not released you can take another one after 5 mint and if the pain also not released you can take another one after 5 mint and if the pain is not reliesed after 5 mint you must to go to emergency beceuse of MI ( acute condition ) 2 ) Stor them away of heat and moisture and light Aspirine • 1) aspirin is give you some protection against recurrence MI or occurring of stroke • 2) if you feel any pain in your stomach or you see blood in the stool you must to tell your doctor

Metoprolol XL • 1) you must to check your pulse daily because this drug reduce the HR 2 ) you may feel dizziness or fatigue Celecoxib We stop using this drug because it increase the risk of MI and stroke ISMN This drug have high tolerance but you take it once daily so no tolerance will occur

Amlodipine We replace diltiazm by this drug because your HR is low and this drug has less effect on HR than diltiazm but may feel some dizziness and fatigue Ranalozine We give you this drug to improve your ischemic condition and this drug has also less effect on BP and HR so this good in your case because your pulse is low and your BP also low May have some nausea and constipation and headache

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Withdrawing aspirin one month after percutaneous coronary intervention (PCI) in high-risk heart patients and keeping them on ticagrelor alone safely improves outcomes and reduces major bleeding by more than half when compared to patients taking aspirin and ticagrelor combined (also known as dual antiplatelet therapy or DAPT), which is the current standard of care.

These are the results from the ULTIMATE-DAPT study announced during a late-breaking trial presentation at the American College of Cardiology Scientific Sessions on Sunday, April 7, and published in The Lancet .

This is the first and only trial to test high-risk patients with recent or threatened heart attack (acute coronary artery syndromes, or ACS) taking ticagrelor with a placebo starting one month after PCI, and compare them with ACS patients taking ticagrelor with aspirin over the same period. The significant findings could change the current guidelines for standard of care worldwide.

"Our study has demonstrated that withdrawing aspirin in patients with recent ACS one month after PCI is beneficial by reducing major and minor bleeding through one year by more than 50 percent. Moreover, there was no increase in adverse ischemic events, meaning continuing aspirin was causing harm without providing any benefit," says Gregg W. Stone, MD, the study co-chair of ULTIMATE-DAPT, who presented the trial results.

"It is my belief that it's time to change the guidelines and standard clinical practice such that we no longer treat most ACS patients with dual antiplatelet therapy beyond one month after a successful PCI procedure. Treating these high-risk patients with a single potent platelet inhibitor such as ticagrelor will improve prognosis," adds Dr. Stone, who is Director of Academic Affairs for the Mount Sinai Health System and Professor of Medicine (Cardiology), and Population Health Science and Policy, at the Icahn School of Medicine at Mount Sinai.

The study analyzed 3,400 patients with ACS at 58 centers in four countries between August 2019 and October 2022. All of the patients had undergone PCI, a non-surgical procedure in which interventional cardiologists use a catheter to place stents in the blocked coronary arteries to restore blood flow. The patients were stable one month after PCI and were on ticagrelor and aspirin. Researchers randomized the patients after one month, withdrawing aspirin in 1,700 patients and putting them on ticagrelor and a placebo, while leaving the other 1,700 patients on ticagrelor and aspirin. All patients were evaluated between 1 and 12 months after the procedure.

During the study period, 35 patients in the ticagrelor-placebo group had a major or minor bleeding event, compared to 78 patients in the ticagrelor-aspirin group, meaning that the incidence of overall bleeding incidents was reduced by 55 percent by withdrawing aspirin. The study also analyzed major adverse cardiac and cerebrovascular events including death, heart attack, stroke, bypass graft surgery, or repeat PCI. These events occurred in 61 patients in the ticagrelor-placebo group compared to 63 patients in the ticagrelor-aspirin group, and were not statistically significant -- further demonstrating that removing aspirin did no harm and improved outcomes.

"It was previously believed that discontinuing dual antiplatelet therapy within one year after PCI in patients with ACS would increase the risk of heart attack and other ischemic complications, but the present study shows that is not the case, with contemporary drug-eluting stents now used in all PCI procedures. Discontinuing aspirin in patients with a recent or threatened heart attack who are stable one month after PCI is safe and, by decreasing serious bleeding, improves outcomes," Dr. Stone adds. "This study extends the results of prior work that showed similar results but without the quality of using a placebo, which eliminates bias from the study."

This trial was funded by the Chinese Society of Cardiology, the National Natural Scientific Foundation of China, and Jiangsu Provincial & Nanjing Municipal Clinical Trial Project.

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Materials provided by The Mount Sinai Hospital / Mount Sinai School of Medicine . Note: Content may be edited for style and length.

Journal Reference :

• Zhen Ge, Jing Kan, Xiaofei Gao, Afsar Raza, Jun-Jie Zhang, Bilal S Mohydin, Fentang Gao, Yibing Shao, Yan Wang, Hesong Zeng, Feng Li, Hamid Sharif Khan, Naeem Mengal, Hongliang Cong, Mingliang Wang, Lianglong Chen, Yongyue Wei, Feng Chen, Gregg W Stone, Shao-Liang Chen, Xiaobo Li, Zhen Ge, Jing Kan, Muhammed Anjum, Fei Ye, Xiaofei Gao, Anjum Jalal, Ping Xie, Ling Tao, Xiang Chen, Hamid S Khan, Asim Javed, Yibin Shao, Xiaomei Guo, Feng Li, Tahir Saghir, Naeem Mengal, Shaoping Nie, Hong Qu, Xuesong Qian, Song Yang, Jing Chen, Dasheng Gao, Lijun Liu, Mingliang Wang, Lianglong Chen, Fan Liu, Tan Xu, Yinwu Liu, Badar Ul Ahad Gill, Qing Yang, Nin Guo, Shangyu Wen, Hongliang Cong, Lang Hong, Imad Sheiban, Afsar Raza, Yongyue Wei, Feng Chen, Gary S Mintz, Jun-Jie Zhang, Gregg W Stone, Shao-Liang Chen. Ticagrelor alone versus ticagrelor plus aspirin from month 1 to month 12 after percutaneous coronary intervention in patients with acute coronary syndromes (ULTIMATE-DAPT): a randomised, placebo-controlled, double-blind clinical trial . The Lancet , 2024; DOI: 10.1016/S0140-6736(24)00473-2

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Date: April 08, 2024    

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