45 year old male.
Medical History

• 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:

• 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.

• 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)

• 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.

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).

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.