volume overload after myocardial infarction) and dilation using the following governing equations:
  
    
      
        F
        =
        
          F
          
            e
          
        
        ⋅
        
          F
          
            g
          
        
        
      
    
    {\displaystyle F=F^{e}\cdot F^{g}\,}
  
where 
  
    
      
        
          F
          
            e
          
        
      
    
    {\displaystyle F^{e}}
   is elastic volume stretch that is reversible and 
  
    
      
        
          F
          
            g
          
        
      
    
    {\displaystyle F^{g}}
   is irreversible, isotropic volume growth described by:
  
    
      
        
          F
          
            g
          
        
        =
        
          I
        
        +
        [
        
          λ
          
            g
          
        
        −
        1
        ]
        
          f
          
            0
          
        
        ⊗
        
          f
          
            0
          
        
        
      
    
    {\displaystyle F^{g}=\mathbb {I} +[\lambda ^{g}-1]f_{0}\otimes f_{0}\,}
  
where 
  
    
      
        
          f
          
            0
          
        
      
    
    {\displaystyle f_{0}}
   is a vector, which points along a cardiomyocytes long axis and 
  
    
      
        
          λ
          
            g
          
        
      
    
    {\displaystyle \lambda ^{g}}
   is the cardiomyocyte stretch due to growth.
Cardiomyocytes reach their maximum length of 150 
  
    
      
        μ
      
    
    {\displaystyle \mu }
  m in the endocardium and 130 
  
    
      
        μ
      
    
    {\displaystyle \mu }
  m in the epicardium by the addition of sarcomeres. Due to the increase in diameter, the dilated heart appears spherical in shape, as opposed the elliptical shape of a healthy human heart. In addition, the ventricular walls maintain the same thickness, characteristic of pathophysiological cardiac dilation. Valvular effects
As the ventricles enlarge, both the mitral and tricuspid valves may lose their ability to come together properly. This loss of coaptation may lead to mitral and tricuspid regurgitation. As a result, those with DCM are at increased risk of atrial fibrillation. Furthermore, stroke volume is decreased and a greater volume load is placed on the ventricle, thus increasing heart failure symptoms. Diagnosis
Generalized enlargement of the heart is seen upon normal chest X-ray. Pleural effusion may also be noticed, which is due to pulmonary venous hypertension.The electrocardiogram often shows sinus tachycardia or atrial fibrillation, ventricular arrhythmias, left atrial enlargement, and sometimes intraventricular conduction defects and low voltage.