Tag Archives: percutaneous coronary intervention

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

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

 

EARLY STENT THROMBOSIS

EARLY STENT THROMBOSIS- AN AUTOPSY STUDY OF LESION CHARACTERISTICS
According to a study published online ahead of print in the Journal of American college of cardiology ,patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) face increased risk of early stent thrombosis in the presence of high thrombus burden with certain pathological traits or suboptimal stenting.

Researchers evaluated 67 stented coronary lesions from 59 patients who presented with ACS and died within 30 days of implantation (between 2004 and 2012).

Early stent thrombosis was identified in 37 lesions from 34 patients (58%), all of whom died of stent-related causes. Of 25 patients without stent thrombosis, cause of death was stent-related in 3 (distal dissection, coronary perforation, and side branch occlusion secondary to stenting). ECG readings at the time of diagnosis revealed STEMI in 16 patients and NSTEMI in 13 patients.

All 33 patients for whom pathological information on the myocardium was available had MI on histologic examination. 

Lesion Characteristics Implicated 

No differences emerged between lesions with (n = 37) or without (n = 30) stent thrombosis in terms of stent location in the coronary tree, duration of the implant, stent type (BMS vs DES or among DES types), number of stents or total stented length, or the underlying pathological findings (eg, plaque rupture, erosion, or calcified nodule).

However, in the stented segment, the maximum index thrombus thickness at the site of greatest thrombus burden was larger and necrotic core prolapse and occlusive thrombus in the side branch were more common in thrombotic lesions compared with patent lesions. Stenting in a false lumen secondary to medial dissection was numerically higher in thrombotic lesions (table 1).

Table 1. Lesion Characteristics: Thrombosis vs Patent

  Thrombosis
(n = 37 lesions)
Patent
(n = 30 lesions)
P Value
Maximum Index Thrombus Thickness, mm 0.22 0.07 0.001
Necrotic Core Prolapse 70% 43% 0.045
Side Branch Occlusion 22% 3% 0.035
False Lumen Stenting 8% 0 0.25


In nonstented segments proximal and distal to the stented segments, severe stenosis (> 75% cross-sectional narrowing), necrotic core prolapse, and medial dissection were more common in thrombotic than patent lesions, but the differences did not reach statistical significance.

 

Comparison of culprit and nonculprit sections within lesions showed that the extent of necrotic core prolapse, medial tear, and incomplete apposition was higher in sections with thrombus.

 

In particular, independent predictors of stent thrombosis on multivariate analysis were:

  • Maximum depth of strut penetration (OR 2.3; 95% CI 1.3-4.3; P = 0.006)
  • Percentage of struts with medial tear (OR 1.8; 95% CI 1.3-2.4; P = 0.001)
  • Percentage of struts with incomplete apposition (OR 1.8; 95% CI 1.4-2.4; P < 0.001)

In addition, plaque rupture was more common in arterial sections with vs without stent thrombosis (OR 2.2; 95% CI 1.5-3.2; P < 0.001).

 

 

Careful Technique, Improved Stent Designs May Help

 

The findings emphasize the potential role of intracoronary imaging in describing the underlying plaque, quantifying the lesion extent, and assessing procedural results in terms of stent apposition.

 

Improvements in stent design may help reduce stent thrombosis risk.

 

Finally, the contribution of thrombus burden to the development of stent thrombosis reinforces the importance of potent antiplatelet and anticoagulant strategies

 

 

Study Details

 

Age, sex, indication for PCI, and past medical history were similar between subjects with and without stent thrombosis.

 

 Sources:

 

1. Nakano M, Yahagi K, Otsuka F, et al. Causes of early stent thrombosis in patients with acute coronary syndrome: an ex vivohuman autopsy study. J Am Coll Cardiol. 2014;Epub ahead of print.

2. Windecker S, O’Sullivan CJ. Mitigating the risk of early stent thrombosis [editial]. J Am Coll Cardiol. 2014;Epub ahead of prin