The heart's blood supply comes from three main arteries: the right coronary artery (RCA), the left anterior descending artery (LAD), and the left circumflex artery (LCX).

• Right Coronary Artery (RCA): Primarily supplies blood to the right ventricle, parts of the septum, and the inferior wall.

• Left Anterior Descending Artery (LAD): Predominantly supplies the anterior wall and apex, with some overlap in perfusion areas.

• Left Circumflex Artery (LCX): Mainly perfuses the lateral wall and parts of the inferior wall.

AIBODY is capable of modeling and calculating the volumes (in blue) and pressures (in black) of all major coronary arteries, as depicted in the image above.

The ECG component within AIBODY generates the ECG waveform to based upon our cellular modelling of physiology and pathophysiology for the supported heart rhythms and arrhythmias.

Within the AIBODY cardiology module, we can simulate the pharmacokinetic and pharmacodynamic effects of a select number of drugs relevant to specific pathologies, such as ventricular tachycardia. By adjusting the dosage, corresponding changes in the ECG and clinical observations will occur, depending on the pathology.

Here is the list of drugs available for simulation:

 • Lidocaine

 • Amiodarone

Defibrillation is a critical medical procedure used to treat life-threatening cardiac arrhythmias, specifically ventricular fibrillation and pulseless ventricular tachycardia. This procedure involves delivering an electric current to the heart via a defibrillator device. The electric shock depolarizes the heart muscles, allowing the sino-atrial (SA) node to restore normal sinus rhythm.

In the AIBODY main module, we can simulate a variety of arrhythmias and the effects of defibrillation at specific voltages. These simulations include the resulting physiological changes and their impact, as demonstrated in the images below.

Myocardial infarction (MI) is pathologically defined as the death of myocardial cells due to prolonged ischemia.  Within the AIBODY Cardio module we can simulate myocardial infarction based upon different coronary artery by selecting the specific distribution and the applying a specific percentage of occlusion of those coronary arteries. 

We simulate the exact changes that occur as a result of myocardial infarction from visualisations of those changes in the 3D model to the ECG changes occurring in real-time.

List of available infarction simulations:

Inferior myocardial infarction involves the inferior wall of the left ventricle, which is typically supplied by the right coronary artery (RCA) or, in some cases, the left circumflex artery (LCx). 

Occlusion of the right coronary artery cause typically causes ST segment changes in the inferior leads (II, III, and aVF) 

Anterolateral myocardial infarction involves the anterior and lateral walls of the left ventricle, which are typically supplied by the left anterior descending (LAD) artery and the left circumflex (LCx) artery. 

Acute anterolateral myocardial infarction refers to ST segment changes within the precordial leads V1–V6 in addition to leads I and aVL.

Apical myocardial infarction affects the apex of the heart, a region that can be supplied by multiple coronary arteries, including the distal left anterior descending (LAD) artery, the left circumflex (LCx) artery, or the right coronary artery (RCA), depending on the coronary anatomy and dominance.

A mid-left anterior descending artery occlusion produces an "apical MI" pattern, characterized by:
  •  ST-segment elevation in precordial leads V3-6.
  •  ST-segment elevation in most of the limb leads.
  •  ST-segment elevation in lead II greater than in lead III.
  •  ST-segment elevation in both leads III and aVL, typically showing reciprocal changes.

Anteroseptal myocardial infarction (MI) involves the anterior and septal regions of the left ventricle, which are primarily supplied by the left anterior descending (LAD) artery. 

An infarct produced by insufficient blood flow via the left anterior descending (LAD) coronary artery and limited to the septal quadrant  is termed an “anteroseptal infarct.” When the infarct extends into the anterior quadrant  and/or into the apical segments of other quadrants, it is commonly referred to as an “extensive anterior” infarct.   

Anteroseptal MI on ECG usually is characterized by the presence of ST-elevations in V1-V3 leads acutely followed by the development of Q waves in V1-V3 precordial leads. 

Posterior myocardial infarction affects the posterior wall of the left ventricle, which is typically supplied by the posterior descending artery (PDA), a branch of either the right coronary artery (RCA) or, less commonly, the left circumflex artery (LCx). 

Posterior wall ST-elevation myocardial infarction commonly occurs as a complication (or extension) of acute inferior wall STEMI. ST-segment depressions appear in the right precordial leads (V1, V2 and V3) with ST-segment elevations in the posterior leads (V7-V9). The precordial ST-segment depressions are the “mirror image” of ST-segment elevations over the posterior left ventricular wall. The culprit infarct-related artery is usually the right coronary artery (RCA) or, less often, the left circumflex artery (LCA).  

Angina is a symptom of coronary artery disease and describes chest pain due to reduced blood flow to the heart. It feels like squeezing, pressure, or heaviness. Angina can be new or recurring and varies by type. 

Stable angina, the most common form, occurs during activity and is relieved by rest or medication. It is predictable and lasts about five minutes or less.
 
AIBODY’s cardio module can simulate various levels of coronary occlusion, showing corresponding changes in coronary perfusion and ECG in both stable and unstable angina. 

Patients with ACS most commonly present with angina, which patients usually describe as pain, pressure, tightness, or heaviness in the chest, with potential radiation to the jaw or left arm. It may be accompanied by shortness of breath, diaphoresis, nausea, or any combination of the above. The chest pain may be precipitated by exertion and relieved by rest and/or nitroglycerin in the case of stable angina.

Patients with stable angina are diagnosed primarily by clinical assessment alone and in some circumstances non-functional assessment with an exercise ECG may be used instead of functional imaging like a stress echocardiogram.

Within AIBODY we can simulate the exercise ECG investigation with patients with stable angina and their corresponding ECG changes seen below.

Sinus tachycardia is a sinus rhythm of the heart where the heart rate is elevated above 100 bpm in an adult. The sinus node generates action potentials, and these impulses are then distributed through the conduction paths to both atria and ventricles and in sinus tachycardia there is an increased discharge from the sino-atrial node. 

Sinus tachycardia ECG features 22 are characterized by:
  •  Presence of P waves that are upright in leads I, II and aVL, and negative in lead aVR;
  •  Each P wave is followed by a QRS and T waves  
  •  Heart rate of greater than 100 beats per minute
 
Within AIBODY cardiology module we simulate sinus tachycardia at the pathophysiological level and the corresponding ECG changes seen in the images below. 

Ventricular Tachycardia (VT) is a broad complex tachycardia which originates from the ventricles. The most common form of ventricular tachycardia is monomorphic VT, which originates from a single focus within the ventricles. Ventricular tachycardia is caused by significant structural heart disease, most commonly coronary artery disease, heart failure and cardiomyopathy.  

We simulate monomorphic ventricular tachycardia within the AIBODY module as seen in the images below.