Acute myocardial infarction with ST segment elevation
Short Summary

45-year-old male with recent extensive anterior ST elevation myocardial infarction that was treated by primary PCI, anticoagulation medications and temporary IABP support. Left ventricular ejection fraction improved with residual hypokinesia. The patient was reported to be in a stable medical condition afterwards and scheduled to undergoing PCI to LCX.

Patient's Questions
  1. Taking into consideration that the test results were substantially normal what could have caused the heart attack? Could the physical effort of the tennis match have been the cause? If so, could this be considered an accident or is it an illness?
  2. Was the emergency treatment necessary? What are the eventual repercussions and consequences of the heart attack? Are there any problems linked to the fact that the thrombus was not aspirated but left in circulation?
  3. Where are the Centres of Excellence in where the next procedure may be performed and future monitoring carried out?
  4. What diet do you advise? What type of exercise do you advise? What kind of lifestyle do you advise?
  5. What periodic checks do you advise in order to avoid a repetition of the problem? If genetic anomalies are confirmed what checks should my family members undergo?
  6. Is it necessary to intervene straight away with regard to the stenosis of the circumflex artery (70%)? Do you agree with the medical treatment prescribed?

 

Medical Background

45 year old male.
Medical History

The patient is a smoker with a family history of ischaemic cardiopathy, arterial hypertension and diabetes mellitus.
Patient states that he was in good health up until the evening of last March when during physical effort (tennis match), he experienced intense oppressive chest pain, with nausea. He was taken to the Emergency Department where an ECG was performed which showed elevation of the ST segment in leads V1 to V5, aVL andinferior ST segment depression. Following administration of ASA, clopidrogel, heparin, and NTG, the patient underwent primary PTCA with the placement of two non-medicated stents in the mid proximal segment of the anterior descending artery. The coronography also showed stenosis of 70% of the circumflex artery mid segment, and a decision was taken to treat this at a later date; the right coronary artery showed no signs of significant stenosis, but slight irregularities to the walls. An aortic counterpulsator was positioned for the presentation of hypotension. Treatment was begun with glycoprotein inhibitors (abciximab). Upon arrival in the Intensive Coronary Care Unit the patient was in fairly good general condition, free from chest pain and dyspnoea, blood pressure 105/50 mmHg, pulse 90 bpm. An echocardiogram was performed which showed that the left ventricle had reduced overall contractility and EF of 35%, akinetic apex, posterior and anterior septum, para-apical segments of the anterior lateral wall.
During the patients stay in hospital the monitor showed episodes of NSVT, pairs of and triple VEB. On the second day after infarction the echocardiogram was repeated and showed substantial improvement in systolic function which was equal to 50%. On March, the IABP was removed, with good haemodynamic compensation.
On March, the patient was transferred to the cardiology ward, asymptomatic and with good circulatory compensation. The haemodynamists and attending cardiologist were contacted and, together with the patient, they decided to complete the procedure of percutaneous revascularization of the circumflex artery after approximately 1 month (planned for April 2008). The patient was discharged on March 2008 clinically stable, without chest pain and dyspnoea and with good circulatory compensation.
The results of the most significant tests carried out during the patient’s stay in hospital are detailed below:
  • Blood tests on admission: Red blood cells 4.6 million, haemoglobin 13.2 g/dl, haematocrit 39%, platelets 274,000, white blood cells 12,670, uraemia 20 mg/dl, creatinine 1.1 mg/dl, sodium 136 mmol/l, total cholesterol 161 mg/dl, HDL 44 mg/dl, LDL 119 mg/dl, triglycerides 38 mg/dl, peak Tnl (15/02): 157 ng/ml, peak CPK-MB (15/02): 430 ng/ml, pro-BNP: 1424 pg/ml.
  • Blood tests on discharge from hospital: creatinine 0.9 mg/dl, potassium 3.7 mmol/l, Tnl: 27.49 ng/ml, CK-MB: 4.5 ng/ml.
  • ECG on admission: Sinus rhythm with average cardiac frequency of 85 bpm, normal atrioventricular and intraventricular conduction. Elevation of ST segment in leads V1 to V5 with inferior ST segment depression.
  • ECG on discharge: See copy attached.
  • Echocardiogram on admission: Left ventricle normal in size with increased thickness of walls. Akinetic apex, posterior and anterior septum and para-apical segments of the anterior lateral wall (Ejection Fraction 35%).
  • Echocardiogram of March 2008: Left ventricle normal size and thickness of walls; systolic function preserved overall (EF 45-50%); hypokinesia of basal and mid segment of anterior IVS and anterior wall; pseudonormal filling. Slight-moderate mitralic insufficiency. IVC of increased calibre (24 mm), barely collapsed on breathing.
  • Coronography and angioplasty:
CORONOGRAPHY DESCRIPTION
    • Left main coronary artery large calibre, absence of lesions.
    • Anterior descending artery large calibre, sub-occlusive stenosis (99%), long, with appearance of endoluminal thrombosis to proximal segment, immediately prior to first diagonal branch. Downward flow TIMI 1-2.
    • Circumflex branch good calibre, atheromatous, shows critical stenosis (70%) of middle segment.
    • Right Coronary artery large calibre, dominant, with slight irregularity of walls along its length, absence of significant stenotic lesions. Initial intercoronary collateral circulation of anterior descending artery.
 
RESULT OF STENTING OF DA
Basal Final
Stenosis: 99% 0%
Diameter reference vessel (mm): 4.0 4.0
MLD:
TIMI flow: 1-2 3
 
Procedure: After having cannulated the left main coronary artery with 6fr EBU 3.75 guide catheter, went past the DA lesion with BMW guide and positioned a second BMW guide distally in the diagonal branch, for protection. Directly implanted BMS Vision 3.5/15 mm released at 14 atm. Subsequently implanted, overlapping, more proximally, a second BMS Vision 4.0/8 mm released at 14 atm. Post-dilatation at embrocation point up to 16 atm. Good final angiographic result with TIMI flow 3.
 
complications
At the end of the procedure an IABP was implanted due to the persistence of low systemic flow.
 
conclusions
Sub-occlusive stenosis of proximal DA. Successful primary angioplasty performed.
 
Treatment advised on discharge:
  • Absolute abstention from smoking;
  • Gradual increase of physical activity, avoiding intense physical effort and emotional stress;
  • Careful control of blood pressure (optimal blood pressure < 130/80 mmHg)
  • Diet low in saturated fat (LDL amount < 70 mg/dl)
 
Drugs:
  • Pariet 20 mg 1 tablet half an hour before breakfast;
  • Triatec 2,5 mg 1 tablet at 8.00;
  • Seloken 100 mg ½ tablet at 8.00 and ½ tablet at 20.00;
  • Plavix 75 mg 1 tablet per day after evening meal for 12 months;
  • Cardioaspirin (Aspirin Cardio) 100 mg 3 tablets per day after lunch for 1 month, then reduce dosage to 1 tablet per day;
  • Torvast 40 mg 1 tablet at 22.00;
  • Lentokalium (translator’s note: active ingredient: potassium chloride; produced by Roche) 1 tablet at 8.00, 1 tablet at 15.00 and 1 tablet at 20.00 for one week only.
 

 

Expert's Opinion

Review of coronary angiogram:The treating interventional cardiologist has done an outstanding job on his LAD during the STEMI event with successful PCI of the LAD and restoration of TIMI 3 flow using 2 BMS implants. The patient should be reassured about the high quality of the work and excellent procedural achievement which was absolutely a 'life saving' one and resulted in clinical stabilization and preservation of his LVEF and most probably improving his overall short and long-term cardiac prognosis (see picture of his pre/post procedure angiographic condition).

 
I tend to agree with the treating cardiologist's recommendation to proceed with subsequent coronary angioplasty procedure of the LCX but someone may argue that the LCX lesion is not critical and could be managed "conservatively" using medications alone and/or based on non-invasive ischemic parameters. Thus, it would be my tendency to postpone the subsequent coronary procedure for ~4 months following the MI event and first re-evaluate the status of the LAD (i.e. +/- restenosis) and only then proceed with CPI of the LCX while trying to preserve the OM branch (bifurcation PCI procedure, see next picture). I would recommend a non-invasive cardiac functional test prior to undertaking the subsequent invasive procedure.
 
The current medications are appropriate and well suited to the clinical situation.
Further responses to Questions:
  1. Taking into consideration that the test results were substantially normal what could have caused the heart attack? Could the physical effort of the tennis match have been the cause? If so, could this be considered an accident or is it an illness? – Heart attack (i.e. acute myocardial infarction) is an unpredictable event on an individual basis so the exact cause should be pre-existing early onset coronary atherosclerosis with flash thrombotic occlusion of the coronary artery. It is unclear whether the physical effort of the tennis match have been the cause (it might have been the case but this is uncertain) and I would consider it a definite illness rather than an accident.
  2. Was the emergency treatment necessary? What are the eventual repercussions and consequences of the heart attack? Are there any problems linked to the fact that the thrombus was not aspirated but left in circulation? – As stated above, the cardiac procedure was absolutely necessary and well performed. The consequence of the heart attack was an impairment of left ventricular function and initial electrical instability that was improved by angioplasty reperfusion although the heart did not resume its normal (pre-infarct) function. In other words, without the urgent angioplasty procedure the clinical situation could have been much worse. The need for coronary aspiration in this case could have been debated and I am not certain it could alter the course of the intervention in this case as the final results was actually very good.
  3. Where are the Centres of Excellence in Rome where the next procedure may be performed and future monitoring carried out? – Since I was impressed by the index procedure I see no reason to alter the choice or place of the subsequent procedure in this case.
  4. What diet do you advise? What type of exercise do you advise? What kind of lifestyle do you advise? - Changes in diet can make a difference. The usual suggestion would be: 1) eat portions of a variety of fruit and vegetables every day, 2) do not eat much fat and/or meat rich in fat and cholesterol, and 3) eat oil-rich fish twice a week. In addition, exercise every day (start by professional guidance and training) and do your best to conduct a non stressful way of living. Maintain a periodic cardiovascular visit at your treating cardiologist. Finally and importantly – never-ever smoke cigarettes !
  5. What periodic checks do you advise in order to avoid a repetition of the problem? If genetic anomalies are confirmed what checks should my family members undergo? – My advice would be to adhere to your cardiologists program of surveillance. It would include periodic stress tests and/or non invasive functional cardiac imaging such as stress echocardiography or SPECT or PET nuclear scans and blood tests for routine blood checks and lipid profile and hypercoagulable state measures and hs-CRP and MTHFR tests. I would also test to aspirin resistance using designated tests (e.g. Acumetrix and/or platelets aggregation studies). Unfortunately there are not concrete genetic tests to be recommended on top of what has already been mentioned above.
  6. Is it necessary to intervene straight away with regard to the stenosis of the circumflex artery (70%)? Do you agree with the medical treatment prescribed? – As stated above I would tend to postpone the LCX intervention by 4 months following the heart attack and re-evaluate the LAD status and do some non invasive tests prior to re-catheterization (such as SPECT nuclear imaging during stress). This would give the advantage to rule out restenosis of the LAD and get a good idea about the functional significance of the LCX lesions prior to intervention. I am in full agreement with the medical treatment prescribed.

 

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