Pathology of dilated cardiomyopathy

2021-01-28 12:00 AM

In the early stages, tachycardia compensates for a decrease in systolic ejection volume in order to maintain cardiac flow (Q = FxV).

Define

Dilated cardiomyopathy is a left ventricular dilatation syndrome with an increase in left ventricular primary volume with an increase in systolic or diastolic function without primary pericardial damage, heart valves or myocardial anaemia.

Clinically dilated cardiomyopathy is characterized by dilation of the two ventricles, the left ventricle is more than the right one, due to a stagnation in the ventricles, which is a source of embolism of blood clots.

In terms of pathology, it is interstitial fibrosis of the heart muscle, hypertrophic and non-specific degenerative muscle cells.

Reason

Some factors are proposed such as Infections (enterovirus), nutrition, poisoning (alcohol), increased BP, damage to coronary microcirculation, immunity, postpartum.

Diagnosis of idiopathic cardiomyopathy: Determined only when known causes have been excluded.

Pathophysiology

Ventricular dilation and contractility: Provide a decrease in ejection index and an increase in end-diastolic volume. This in turn reduces atrial emptying, increases left atrial pressure and left ventricular end-diastolic pressure. In the early stages, tachycardia compensates for a decrease in systolic ejection volume in order to maintain cardiac flow (Q = FxV). Thereafter, a decrease in cardiac output, an increase in pulmonary capillary pressure (OAP) and, ultimately, an increase in pulmonary capillary pressure and right ventricular failure appears.

A decrease in renal perfusion pressure: Provides stimulation of the remine - angiotensin - aldosterone system. This increases blood volume but causes peripheral vasoconstriction. Sub-endocardial anaemia is common due to a decrease in coronary reserve.

clinical

Asked the disease

Prehistoric:

Current or past personal history and treatment.

Family.

Mechanical symptoms:

Fatigue, shortness of breath of degrees.

Peripheral oedema, chest pain, palpitations, history of peripheral or cerebral embolism.

Clinical examination

Heart: Tachycardia, normal or low arterial blood pressure, left-sided apex, T3, T4 tones, cleft and/or tricuspid systole, signs of RV failure.

Lungs: Pulmonary, pleural effusion.

 

Subclinical

Chest X-ray: Heart enlarged with an increase in heart/chest ratio, a sign of pulmonary congestion, pleural effusion.

Electrocardiogram: Sinus tachycardia, non-specific ST-T segment abnormalities, left ventricular hypertrophy, incomplete or complete left bundle branch block, atrial abnormality, decreased amplitude R wave. Sometimes Q waves can easily confuse myocardial necrosis, atrial arrhythmias and ventricular rhythm.

Biochemistry: Reduced blood sodium, functional renal failure, normal CPK.

Echocardiography:

Ultrasound of 2 cells of the heart and IV: Dilating the heart chambers, especially the left ventricle, reducing the plasticity index, reducing the contractility of the entire heart wall, sometimes without contractility, easily causing the coronary failure, blood clots and overflow pericardial fluid.

Cardiac Doppler: Find a 2-leaf open (functional), 3-leaf open or pulmonary artery regurgitation, the

diastolic dysfunction, assessment of cardiac output.

Special exploration methods:

Myocardial flicker: The ejection index decreases.

Cardiac catheterization: Allows the assessment of chamber pressure, the heart chambers, the heart valves. Myocardial biopsy is only needed when trying to find the cause.

Holter rhythm, exercise test, heart stimulation.

Evolution

Complications: Total heart failure, atrial fibrillation, ventricular tachycardia and sudden death, peripheral embolism and brain, lung.

Median survival: 6 months to 3 years after the onset of symptoms, 20% of patients have a more favourable course.

Differential diagnosis

Progressive ischemic cardiomyopathy.

Cardiomyopathy caused by progressive hypertension.

Heart valve disease, especially severe mitral regurgitation.

Obstructive cardiomyopathy.

In general, primary dilated cardiomyopathy is diagnosed when it is ruled out after excluding all causes of left ventricular dilatation, especially severe coronary artery disease or severe cleft palate.

Treatment

General measures

Rest when you have heart failure attacks (T).

Salt diet.

Quit alcohol, heart poisoning drugs and reduce heart contractions.

Drug treatment (in addition to pulmonary oedema):

Combined with vasodilator and diuretic type.

ACE inhibitors: A group considered to be the most effective for reducing mortality from heart failure (NYHA stages III and IV).

Dihydrazine-Nitrés derivative combination: Can be used but uncomfortable because of high doses.

Anticoagulant with vitamin K anticoagulants: In the absence of contraindications, it is used in the case of severe ventricular dilatation with a change in the function of cardiac contractility, intraventricular clots, history of embolism.

Many treatment regimens are being evaluated such as Vasodilators combined with inotropic drugs.

Beta-blockers: Need to be used in the hospital provided that there are no contraindications, heart stimulation and low dose should be used after the gradual increase.

Treatment of complications

Pulmonary oedema.

Shock: Using drugs to increase heart contractions (stimulant group (: Dobutamine, Dopamine)

Atrial fibrillation: Digital and/or amiodarone. Antiarrhythmic drugs of groups IA and IC are not used.

Ventricular arrhythmia: amiodarone.

Heart transplant:

Treatment of common dilated cardiomyopathy

Cardiomyopathy caused by alcoholism: Alcohol withdrawal, classic whole heart failure treatment, vitamin B rich intake. Only a few patients can survive within 3 years without alcohol withdrawal and timely treatment.

Perinatal cardiomyopathy: Treatment like generally dilated cardiomyopathy ... Note to stop birth to avoid relapse.

Treatment of obstructive cardiomyopathy (Gallbladder disease)

Contraindicated to the following measures

Strenuous, heavy sports (sudden death).

Digital.

Nitrate derivatives (unless associated coronary failure) and simple types of dilatation of the arteries.

Isoproterenol and sympathomimetics (Dopamine, dobutamine).

Specific treatment

Medicines: No change in sudden death rate.

Beta blockers: Propranolol (Avlocardyl 160-320 mg / day) may provide 30-35% symptom relief.

Calcium preparations:

Verapamil (Isoptin 360 ​​mg/day): symptom improvement when there is no beta-blocker response, but there are many complications (hypotension, sinus node disorder, NT block ...), so it is only used in hospital

Disopyramide (Rythmodan): Beneficial because it reduces arrhythmias, reduces contractility, reduces congestion.

Amiodarone (Cordarone): Reduces signs of functional use when the above drugs fail or when a severe ventricular arrhythmia occurs.

Surgical treatment:

Cardiomyopathy of the basal septum.

Change of mitral valve: when the surgery is not good, the death rate from surgery is 5-8%, the result is nearly 90% from 6 months to 1-year, long term is only 70% in 5 years.

Point:

Asymptomatic obstructive cardiomyopathy in young people.

Treatment with an an-blocker or verapamil is indicated when

Family history of sudden death.

Clear left ventricular hypertrophy.

The contraction in the left ventricular chamber.

Clinical monitoring is required every 3 months and ultrasound every 6-12 months.