Ventricular wall tumor of the left ventricle

  【Overview】.
  The above ventricular wall tumors occur on the basis of coronary heart disease and myocardial infarction.
  They are most common in the anterolateral wall, apical and anterior part of the septum of the left ventricle (left anterior descending branch infarction), and rare in the posterior wall (left circumflex branch or right posterior descending coronary artery infarction).
  One-third of ventricular wall tumors have wall-attached thrombi.
  The prognosis is poor, with a 5-year survival rate of 12% (10%-24%) in patients with symptomatic ventricular wall tumors.
  The causes of death are, in order, ventricular arrhythmias, heart failure, recurrent myocardial infarction, and embolism of the body circulation.
  In recent years, the incidence of left ventricular wall tumors has decreased significantly due to aggressive medical therapy such as thrombolysis and revascularization.
  [Etiology].
  After myocardial infarction, the myocardium in the infarcted region lacks timely and effective establishment of collateral circulation.
  Pathology
  True ventricular wall tumor.
  The non-contractile ventricular wall in the infarcted area is replaced by fibrous scar tissue that bulges outward, accompanied by a bulging ventricular cavity.
  The tumor wall contains some cardiomyocytes.
  Pseudoventricular wall tumor.
  Small perforations within the myocardial infarction zone are formed by adhesions and encapsulation of their surrounding pericardium.
  The wall does not contain cardiomyocytes.
  It is a type of rupture of the left ventricular wall.
  It has a tendency to rupture and should be repaired surgically in time.
  Pathophysiology]
  When the heart is systolic, the pressure in the left ventricle rises and some of the blood in the left ventricular cavity is injected into the enlarged tumor capsule, causing a decrease in the left ventricular blood discharge.
  During diastole, the left ventricular pressure decreases, the ventricular wall bursa shrinks, and some of the blood in the bursa flows back into the left ventricular cavity, which increases the left ventricular preload.
  The left ventricular volume increases, the end-diastolic pressure rises and is large, and the left edge of the heart is locally dilated or has abnormal margins.
  Fluoroscopy: weakened heart beat, reverse left ventricular pulsation.
  Echocardiography: High sensitivity and specificity for definitive diagnosis. It shows reduced ventricular wall motion and segmental contradictory motion. To understand the location and size of the tumor, the presence or absence of wall thrombus, septal perforation and mitral valve incompetence in the tumor capsule.
  Ancillary tests
  ECG: anterior wall pathological Q wave, ST segment continuous elevation. v1-3ST≥0.3mV or V4-6ST≥0.1mV has diagnostic significance.
  Myocardial nuclear scan: show the extent of ventricular wall tumor and ventricular wall systolic function.
  Left ventriculography: definitive diagnosis. It shows: the location, size and presence of attached thrombus in the wall of ventricular wall tumor; left ventricular ejection fraction; unaffected left ventricular wall contractility; whether there is coexisting mitral valve insufficiency and ventricular septal perforation.
  Coronary angiogram: showing coronary artery obstructive lesions.
  [Diagnosis
  History of coronary heart disease and myocardial infarction.
  Angina pectoris, dyspnea, palpitations, syncope, and a sense of dying.
  The apical pulses were diminished, the heart borders were enlarged, and systolic blowing murmurs were heard in the apical region.
  Echocardiography, left ventriculography and other examinations to understand the location and size of ventricular wall tumor, the presence of attached thrombus in the tumor capsule, septal perforation and mitral valve closure insufficiency, etc.
  Treatment
  Conservative treatment: asymptomatic patients with ventricular wall tumors.
  Surgical treatment.
  The purpose of surgery: to remove the fibrous scarred tumor wall, remove the attached wall thrombus, and restore the enlarged ventricular cavity so as to improve cardiac function and myocardial blood supply.
  Surgical indications.
  Intractable heart failure, refractory malignant ventricular arrhythmias, angina pectoris, progressive enlargement of the tumor and recurrent embolism of the body circulation.
  Pseudoventricular wall tumors have a tendency to rupture and should be repaired surgically in a timely manner.
  Contraindications to surgery.
  Ventricular wall tumors that exceed 50% of the left ventricular wall and have a small ventricular cavity after resection.
  Giant ventricular wall tumors with generally low contractility of the unaffected ventricular wall and failure to improve postoperative cardiac function.
  Timing of surgery: If the condition allows, it is appropriate to operate 3 months after myocardial infarction. At this time, the infarcted myocardium is fibrotic and the incision is firmly sutured.
  Surgical methods.
  Ventricular wall tumor resection (for anterior lateral wall and apical ventricular wall tumor).
  Left ventricular cavity patching (for giant ventricular wall tumors in the anterior lateral wall).
  Foldoplasty (for small apical ventricular tumors without wall thrombus).
  Circular patch angioplasty (for inferior or posterior wall ventricular wall tumors).