Tag Archives: coronary artery disease

Myocardial Infarction- Third Universal definition and classification

Definition of myocardial infarction

Criteria for acute myocardial infarction :

The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Under these conditions any one of the following criteria meets the diagnosis for MI:

Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following:

  1. Symptoms of ischaemia.
  2. New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB).
  3. Development of pathological Q waves in the ECG.
  4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
  5. Identification of an intracoronary thrombus by angiography or autopsy.

•Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained,or before cardiac biomarker values would be increased.

• Percutaneous coronary intervention (PCI) related MI is arbitrarily defined by elevation of cTn values (>5 x 99th percentile URL) in patients with normal baseline values (≤99th percentileURL) or a rise of cTnvalues >20% if the baseline values are elevated and are stable or falling. Inaddition,either(i)symptoms suggestiveof myocardialischaemia or (ii) new ischaemic ECG changes or (iii) angiographicfindings consistent with a proceduralcomplication or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

• Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL.

• Coronary artery bypass grafting (CABG) related MI is arbitrarily defined by elevation of cardiac biomarker values (>10 x 99th percentile URL) in patients with normal baseline cTn values (≤99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB,or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

Criteria for prior myocardial infarction

Any one of the following criteria meets the diagnosis for prior MI:

• Pathological Q waves with or without symptoms in the absence of non-ischaemic causes. • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract,in the absence of a non-ischaemic cause.

• Pathological findings of a prior MI

 UNIVERSAL CLASSIFICATION OF MYOCARDIAL INFARCTION

Type 1: Spontaneous myocardial infarction

Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD but on occasion non-obstructive or no CAD.

Type 2: Myocardial infarction secondary to an ischaemic imbalance

In instances of myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g.coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anaemia, respiratory failure, hypotension, and hypertension with or without LVH.

Type 3: Myocardial infarction resulting in death when biomarker values are unavailable

Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.

Type 4a: Myocardial infarction related to percutaneous coronary intervention (PCI)

Myocardial infarction associated with PCI is arbitrarily defined by elevation of cTn values >5 x 99th percentile URL in patients with normal baseline values (£99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial chaemia, or (ii) new ischaemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no-flow or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

Type 4b: Myocardial infarction related to stent thrombosis

Myocardial infarction associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/ or fall of cardiac biomarkers values with at least one value above the 99th percentile URL.

Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG)

Myocardial infarction associated with CABG is arbitrarily defined by elevation of cardiac biomarker values >10 x 99th percentile URL in patients with normal baseline cTn values (£99th percentile URL).In addition,either (i) new pathological Q waves or new LBBB,  or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

Top 10 Cardiology Articles of the week

Top 10 Cardiology Articles of the week  (24.11.14 – 30.11.14)

1. Transcatheter Closure of Large Atrial Septal Defects: Feasibility and Safety in a Large Adult and Pediatric Population

Conclusions—Closure of large atrial septal defects using the Amplatzer device is safe and effective in both adults and children. Superior and posterior rim deficiencies are associated with procedural failure. Closure can be performed under transthoracic  echocardiographic guidance in experienced centers. Early device migration is rare and can be safely managed by device extraction.  Long-term follow-up showed no deaths or major late complications in  311 patients.

2. Stent Coverage and Neointimal Proliferation in Bare Metal Stents Postdilated With a Paclitaxel-Eluting Balloon Versus Everolimus-Eluting Stents: Prospective Randomized Study Using Optical Coherence Tomography at 6-Month Follow-Up

Conclusions—Good stent strut coverage of >94% was found in both therapy groups. Despite greater suppression of global neointimal growth in DES, both DES and BMS+DEB effectively prevented clinically relevant focal restenosis at 6-month follow-up.

3. Multicenter Evaluation of a Next-Generation Balloon-Expandable Transcatheter Aortic Valve
Conclusions – This third-generation device addresses major deficiencies of earlier valves in terms of ease of use, accuracy of positioning, and paravalvular sealing. The rates of mortality and stroke with transfemoral access are among the lowest reported and support further evaluation as an alternative to open surgery in intermediate-risk patients.
(Safety and Performance Study of the Edwards SAPIEN 3 Transcatheter Heart Valve [SAPIEN3]; NCT01808287)

4. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation

5. Percutaneous Left Atrial Appendage Closure: Procedural Techniques and Outcomes

6. Atenolol versus Losartan in Children and Young Adults with Marfan’s Syndrome

Conclusion – Among children and young adults with Marfan’s syndrome who were randomly assigned to losartan or atenolol, no significant difference was found in the rate of aortic-root dilatation between the two treatment groups over a 3-year period.

7. Inactivating Mutations in NPC1L1 and Protection from Coronary Heart Disease

Conclusion – Naturally occurring mutations that disrupt NPC1L1 function were found to be associated with reduced plasma LDL cholesterol levels and a reduced risk of coronary heart disease.

8. MagnaSafe: MRI safe for patients with pacemakers, ICDs

9. Catheter Ablation of Atrial Fibrillation in Patients with Left Ventricular Systolic Dysfunction: A Systematic Review and Meta-Analysis

10. Long-term Clinical and Angiographic Outcomes of the Mini-STAR Technique as a Bailout Strategy for Percutaneous Coronary Intervention of Chronic Total Occlusion

Extended-Release Niacin with Laropiprant

HPS2-THRIVE trial

Among patients with atherosclerotic vascular disease, the addition of extended-release niacin–laropiprant to statin-based LDL cholesterol–lowering therapy did not significantly reduce the risk of major vascular events but did increase the risk of serious adverse events.  

Effects of Extended-Release Niacin with Laropiprant in High-Risk Patients — NEJM.

cpr

Sudden cardiac death

What is sudden cardiac death (SCD) ?

Sudden cardiac death is defined as natural death from cardiac causes, heralded by abrupt loss of consciousness within 1 hour of the onset of an
acute change in cardiovascular status. Related terms are sudden cardiac arrest and cardiovascular collapse. Sudden cardiac arrest means abrupt cessation of cardiac
mechanical function, which may be reversed by prompt intervention but will lead to death in its absence. Cardiovascular collapse means sudden loss of effective
blood flow due to cardiac and/or peripheral vascular such as cardiac arrest or syncope.

What is the relation to heart disease?

preexisting heart disease may or maynot have been known to be present. The mode of death is natural rapid and unexpected.

What are the symptoms?

Prodromes occuring weeks or months before an event are not very accurate to predict SCD. Sudden onset of chest pain, dyspnea, palpitation, lightheadedness
often precede the onset of cardiac arrest and eventual death.

How big is the problem?

For an adult population 35 years of age and older, the overall incidence of sudden cardiac death is 0.1% to 0.2% per year (that means in a country like India
12,00,000 to 24,00,000 people die suddenly from natural cardiac causes each year). Among people who have disease of coronary arteries of heart around 50% die
suddenly and unexpectedly. Even in developed countries where there is a decrease in total number of deaths due to coronary artery disease, the proportion of
deaths that are sudden and unexpected has remained same. These examples highlight the extent of the problem.

Who are at increased risk?

The conditions increasing the risk of sudden cardiac death are

  1. Coronary artery disease- Myocardial infarction, Angina etc
  2. Myocardial diseases and heart failure- e.g. dilated cardiomyopathy, ischemic cardiomyopathy etc
  3. Hypertrophy of ventricular myocardium – hypertrophic cardiomyopathy, left ventricular hypertrophy due to hypertension, etc
  4. Inflammatory diseases of heart- viral myocarditis, sarcoidosis, amyloidosis,
  5. Arrhythmogenic right ventricular dysplasia
  6. Diseases of cardiac valves- Aortic stenosis/insufficiency, mitral valve prolapse
  7. Electrical diseases of heart – long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation etc.
Mechanism of Sudden death

In 80% of cases sudden cardiac death is caused by ventricular tachycardia (VT) or ventricular fibrillation (VF) and in 20% of cases
SCD is caused by bradycardia. Patients having tachycardia have a relatively better outcome and chances of survival than those having bradycardia.

Management

The acute management of cardiac arrest is cardiopulmonary resusitation. More information about latest guidelines of CPR can be found
here

Prevention

Prevention of SCD is divided into two parts: Secondary prevention and Primary prevention. Secondary prevention means preventing further cardiac arrest
in people who have survived one cardiac arrest. Primary prevention means preventing cardiac arrest in people who have rish factors for cardiac arrest
but so far haven’t suffered a cardiac arrest.
Implantable cardioverter-defibrillator(ICD) is a device shown to be effective in secodary and primary prevention of SCD. This device is implanted like
a pacemaker and it gives an electrical shock from inside of the heart to abort an episode of VT or VF. It also has pacing function to support when the
heart rate falls.
Clinical trials like AVID, CASH, CIDS have shown effectiveness of ICD in secondary prevention of SCD. Clinical trials like MADIT, CABG-Patch, MUSTT, DEFINITE and
SCD-HeFT have shown benefit odf ICD in SCD.
Many modifications of the device has come like- subcutaneous ICD and wearable ICD.

Electrophysiological study
EPS and radiofrequency ablation can be done in selected patients to prevent further episodes of cardiac arrest.

Summary: sudden cardiac death is a devastating event resulting in rapid, unexpected and natural death due to cardiac causes. It can occur in persons
with known or unknown heart disease. Effective therapies are available. Increasing awareness about the condition and early therapy can result in
reduction of risk of sudden cardiac death
Keyword: Sudden cardiac death, sudden cardiac arrest, implantable cardioverter defibrillator (ICD), coronary artery disease, heart failure, heart disease, cardiology.

Percutaneous ventricular restoration therapy

Percutaneous ventricular restoration therapy

This is a new form of device therapy for heart failure. The device used is Parachute implant® (http://www.cardiokinetix.com/).

Parachute implant is an umbrella shaped device that is inserted into the left ventricle.

Pathophysiological basis of use:

–          In post MI patients there is progressive LV remodelling (progressive dilatation of the               left ventricle).

–          This dilatation of the ventricle increases the LV wall stress.

wall stress = (LV pressure  × LV diameter)÷  ( 2×LV wall thickness )

–          Increased LV wall stress increases LV afterload

–          Increased LV afterload worsens the LV dysfunction.

What the device does:

This device is useful in patients with old anterior and antero-apical infarctions and LV             dysfunction.

–          Parachute implant separates the dilated apical portion of the left ventricle from the                 normally contracting LV.

–          There by improves the LV geometry

–          Reduces the LV afterload

–          Improves LV function

Data regarding efficacy:

In a recent study presented at ESC heart failure congress,

–          There was a significant reduction in LV end-diastolic (120.8 vs 103.8) an end-systolic volumes (87.6 vs 73.2) at 12 months after parachute implant. There was significant increase in LVEF (28.4 vs 30.4).

–          Symptomatic improvement

–          Improvement in functional class

–          It might improve heart failure related admissions and mortality.

Risks:

–          Interference of the device with papillary muscles or apical chordae tendineae is unknown

–          Risks and consequences of dislocation.

–          Thrombo-embolic risk.

Ongoing Trials:

PARACHUTE IV

 Conclusion:

This device represents a percutaneous alternative for LV reduction surgeries. Long term safety and efficacy results to be seen.

APPOSITION IV : Trial

STENTYS SELF APPOSITION SES:

It is a self-expandable sirolimus-eluting coronary stent system, similar in concept to other self-expanding systems.

Watch the video:

Stentys self-apposition SES

APPOSITION IV trial:

Patients – 152 patients presenting with STEMI.

Design: Patients were randomized to Stentys self-apposing SES (Stentys, Paris, France; n = 90)   vs Resolute zotarolimus-eluting stent (ZES; Medtronic, Santa Rosa, CA; n = 62). Each treatment arm was then randomized to either 4- or 9-month follow-up.

 -Results: On QCA, no differences were observed between the treatment arms just after the procedure for in-stent minimal and mean lumen diameter. In-stent mean lumen diameter was larger at both 4- and 9-month follow-up for Stentys compared with Resolute (3.39 ± 0.46 mm vs 3.13 ± 0.35 mm).

-OCT demonstrated that Stentys SES was associated with fewer malapposed struts (0.07 ± 0.26% vs 1.16 ± 1.59%) and more covered struts (94.32 ± 5.69% vs 89.09± 5.65%) than Resolute ZES at 4 months. Percentage of stents with all struts covered was also higher with Stentys compared to Resolute ZES (33.3% vs 3.8%).

-No differences in malapposition (P = .55) or coverage (P = .81) were seen between the treatment arms in the 9-month cohort.

-Clinical outcomes were low and well balanced between stent groups in terms of MACE (P = .46), TVF (P = .46), and target vessel MI (P = .39).

-Predilatation Needed.

-The device is larger in profile as compared to DES

 Conclusion: Stentys, a self-apposing sirolimus-eluting stent (SES), shows ‘excellent’ apposition over time—better than an existing balloon-expandable drug-eluting stent—in patients with ST-segment elevation myocardial infarction (STEMI). The newer device is associated with faster strut coverage.

Your comments and insight most welcome

 

Coronary artery disease

Coronary artery disease

The heart like any other organ in the body needs constant supply of blood to survive. Blood reaches different parts of the heart through the coronary arteries.  Coronary arteries are of vital importance for the sustenance of life.

The different  normal functions of the coronary arteries include:

1. Carrying blood to different  parts of the heart

2. Regulating  blood supply to the heart in the face of varying blood pressure

3. Increasing blood supply to the heart in the face of increased cardiac demand like during exercise.

The coronary arterial system:  Can be divided into four parts

1. Left main coronary artery (LMCA)

        Which divides into

2. Left anterior descending artery  (LAD) And

3. Left circumflex artery (LCX)

4. Right coronary artery (RCA)

LMCA

Left main coronary artery, left anterior descending and left circumflex coronary artery

RCA

Right coronary artery

What is coronary artery disease (CAD)

Any disease which involves coronary arteries is CAD. Usually the most common form is reduction in the size of the coronary arteries. Many disease conditions can result in coronary artery disease but the most common cause of CAD is atherosclerosis. Other diseases like autoimmune diseases, congenital diseases can result in CAD.

Why CAD occurs?

CAD occurs due to a variety of reasons, which are called risk factors. You can read more about risk factors here.

What are the types of CAD?

CAD is a septum of diseases and it is divided to two categories

1. Chronic stable angina (CSA): In CSA there is a pattern of chest discomfort associated with exertion or emotional excitability. The occurrence of angina is after a predictable amount of work.

2. Acute coronary syndromes ( ACS)

ACS are are again divided into three types

A. Unstable angina: When there is new onset angina, worsening of previous angina, rest angina, it is called unstable angina

B. Non-ST elevation myocardial infarction

C. ST elevation myocardial infarction – the classic heart attack

This classification is important for the point of view of management and the aggressiveness of treatment.

What are the symptoms of coronary artery disease?

 A. Angina : Chest pain or discomfort .

B. Angina equivalents – fatigue , dyspnoea (shortness of breath) , eructations, palpitation

C. Sudden onset acute severe chest pain

D. Cold sweating

Read more about symptoms of heart disease here.

What to do?

First of all see your doctor for evaluation and treatment. Some of the general management modalities are discussed here.

Investigations

For the diagnosis of CAD the following investigations may be needed:

A. ECG – is of central importance in CAD. ECG in many occasions shows changes suggestive of reduced myocardial blood flow

B. Stress test – Different types of stress tests are available like treadmill test, nuclear stress  tests. A stress test can be done by performing exercise on a treadmill or by giving drugs in patients who are unable to do exercise. It is done when the symptoms are not typical and ECG changes are not typical.

C. Echocardiography – is for assessment of structure and function of heart

D. CT coronary angiography – It  is a noninvasive imaging modality for the diagnosis of CAD. It is like any other CT scan. Contrast injections are given to visualize the coronary arteries

E. MRI coronary angiography – Not very widely used for imaging of coronary arteries

F. Coronary angiography – this is the gold standard for the diagnosis of coronary artery disease and any percutaneous treatment for CAD can be done in the same setting

Treatment:

A. Risk factor control – Risk factor control is one of the most effective interventions for reducing the impact of coronary heart disease.  Proper control of blood pressure, diabetes, quitting smoking, treatment of abnormalities of cholesterol are some of the steps that greatly reduce the incidence and prevalence of CAD.

B. Medications- Patients with CAD will on some medications indefinitely (usually life long). For chronic stable angina, the first line of treatment is usually medical management. Even  patients who undergo coronary artery stenting or bypass surgery need to take medicines life long.

C. Coronary angiography and percutaneous coronary interventions are usually advised for patients who have more serious symptoms or for whom symptoms are not easily controlled with medicines. In presence of certain high risk factors patients should undergo early angiography and intervention or surgery

D. Coronary artery bypass grafting (CABG)

Drugs used in treatment of CAD:

1. Anti- platelets e.g. Aspirin, Clopidogrel, Prasugrel, ticagrelor, etc

2. Statins e.g. rosuvastatin, atorvastatin etc

C. Beta blockers (metoprolol, bisoprolol etc)

D. Ace inhibitors or angiotensin receptor blockers

E. Anticoagulants (heparin)

F. Nitrates

G. Nikorandil

H. Ranolazine

I. Trimetazadine

H. Therapies for refractory angina

Details about each class of drug I will post each week( Monday )

So please follow up

Cardiac interventions for CAD:

Known as percutaneous coronary intervention(PCI). In this procedure coronary angiography is done and then stenting is done as required.

Coronary artery bypass grafting:

CABG may be needed where PCI is not feasible or doesn’t give optimum results.

Finally there are a spectrum of patients who have drug refractory angina who are not suitable for PCI or CABG. They have refractory angina and the treatment options are limited in such patients.

Conclusion: Coronary artery disease is the leading cause of death and suffering in the world. The most common symptoms include chest pain, shortness of breath. It is diagnosed by ECG, stress tests, coronary angiography etc. The treatment include risk factor reduction, medical management and PCI or bypass surgery as needed.

Key words: Patient information, Coronary artery disease, heart disease, coronary angiography, ECG, Angina, CAD, PCI, CABG

Vorapaxar (Zontivity) approved

CardioSource – FDA Approves Vorapaxar to Reduce Heart Attack and Stroke Risks in HighRisk Patients.

The U.S. Food and Drug Administration (FDA) has approved vorapaxar (Zontivity) to reduce the risk for MI, stroke, cardiovascular-related death and coronary revascularization among patients who have previously experienced MI or peripheral artery disease.

Vorapaxar is the first in a new class protease-activated receptor-1 (PAR-1) antagonist drugs

targets thrombin-induced platelet activation.

In patients who have had a heart attack or who have peripheral arterial disease, this drug will lower the risk of heart attack, stroke, and cardiovascular death.

In the study that supported the drug’s approval, Zontivity lowered this risk from 9.5 percent to 7.9 percent over a 3-year period – about 0.5 percent per year.

Adverse effects include excess bleeding and easy bruisability

A 2011 clinical trial (TRA 2P-TIMI 50 Presentation Slides (Morrow))showed vorapraxar, added to other anti-platelet agents (generally aspirin and clopidogrel), reduced the rate of a combined endpoint of heart attack, stroke, cardiovascular death, and coronary revascularization when compared to placebo.