Postinfarction Ventricular Septal Rupture - Causes, Symptoms, Diagnosis, and Treatment

Introduction:

The heart has four chambers- two upper sections, the right and left atrium, and two lower sections, the right and left ventricles. Parallel to four chambers, the heart has four valves: mitral, tricuspid, aortic, and pulmonary. Valves are a crucial part of the heart’s structure. They open and close as the blood passes through them. They mainly regulate the entry and exit of blood into the heart’s various chambers. The valves have flaps or leaflets that open and close. Valves with three leaflets open and close simultaneously. In order to avoid any sort of backflow of blood, the leaflets close, and vice versa is why they open.

Myocardial infarction is also commonly referred to as a heart attack. Heart attack is an exceedingly dangerous condition for an individual. There is an absence of blood flow to the muscles of the heart during a myocardial infarction. The reason for this lack of blood flow varies from different factors to different underlying conditions. However, blockage of the heart arteries is generally one of the most common causes of a heart attack or a myocardial infarction or MI. During this, one or more areas of the heart are devoid of blood and thus oxygen. Postinfarction ventricular septal rupture is one of the dreaded complications that lead to a high rate of morbidity as well as mortality in patients, especially those suffering from acute ST-elevation myocardial infarction.

What Are the Causes of Postinfarction Ventricular Septal Rupture?

Postinfarction ventricular septal rupture or PSVR has a higher potential to develop in those patients who are above 65 years of age, female gender, have a history of hypertension, have a diagnosed chronic illness of the kidney, and have no known history of a habit of tobacco or smoking. Postinfarction ventricular septal rupture generally occurs after the episode of a first heart attack or myocardial infarction, MI after a huge delay, or the absence of reperfusion therapy.

Angiography is used to reveal the absence of smooth circulation in and out of the infarct zone. Since the previous or the initial episode of heart attack with ischemia will induce myocardial preconditioning along with a decrease in the transmural myocardial necrosis and rupture of the septum of the heart, the patients with a history of diabetes mellitus, chronic stable or unstable angina, and a history of myocardial infarction, are generally less susceptible to experience a postinfarction ventricular septal rupture. Postinfarction ventricular septal rupture can develop anywhere between one week to two weeks after an acute ST-elevation myocardial infarction, with a peak in the initial twenty-four hours up to five days after the heart attack.

What Are the Signs and Symptoms of Postinfarction Ventricular Septal Rupture?

Postinfarction ventricular septal rupture occurs in approximately one to three percent of the patients who are suffering from acute ST-elevation myocardial infarction but not with reperfusion therapy. The condition is also found in only a mere 0.2 to 0.34 percent of individuals who have received fibrinolytic therapy. Among those patients who underwent reperfusion therapy, postinfarction ventricular septal rupture is reported to be observed at a higher rate than those who have undergone fibrinolytic therapy. Postinfarction ventricular septal rupture is additionally reported after percutaneous coronary intervention as well as cardiogenic shock. Mentioned below are a few of the signs and symptoms of postinfarction ventricular septal rupture.

• Repeated episodes of angina.

• Pulmonary edema and swelling.

• Hypotension (abnormally low blood pressure).

• Cardiogenic shock (a life-threatening condition where the heart is unable to pump enough blood to meet the body's demands, resulting in a severe drop in blood pressure and organ dysfunction).

• Hemodynamic compromise (an impaired or unstable circulatory system).

• Biventricular failure (a condition where both the left and right ventricles of the heart are unable to pump blood effectively).

• Abnormal heart sounds and murmurs.

• Sweating.

• Pale skin.

• Cool hands and extremities.

• Shortness of breath.

• Chest pain gets worse over time.

• Severe pressure on the chest.

• The feeling of fullness.

• Pain and squeezing sensation in the chest.

• Discomfort or pain in the middle of the chest, right and left shoulders, and jaws.

• Pain or tightness in the neck.

• Nausea.

• Vomiting.

• Dizziness.

• Fainting.

• Fatigue.

• Lightheadedness.

• Weakness.

• Rapid pulse.

• Unexplained wheezing.

• Anxiety.

• Stomach pain.

• Severe crushing, like chest pain.

• Insomnia (sleeplessness).

• Malaise.

• Anxiety.

• Nervousness.

• Tremors.

• Pale skin.

• Chest pain while climbing stairs.

• Bluish discoloration of the lips and nails.

How to Diagnose Postinfarction Ventricular Septal Rupture?

The available diagnostic tools that allow measuring the intensity, as well as the presence of postinfarction ventricular septal rupture, are- electrocardiogram, transthoracic echocardiogram, right heart catheterization, left heart catheterization, cardiac magnetic resonance imaging, and cardiac computed tomography. All these tests aid in the diagnosis of the rupture by analyzing its size, location, angulation, and several other vital determinants of mortality. The oxygen saturation of the pulmonary artery is additionally monitored through these diagnostic tools. It should be noted that a combination of all the above-mentioned diagnostic measures has proven to be exceptionally helpful in hemodynamically unstable patients suffering from postinfarction ventricular septal rupture.

How to Treat Postinfarction Ventricular Septal Rupture?

Invasive monitoring is one of the most highly recommended treatment options parallels the measurement of both- right and left ventricles and their filling pressures so that it serves as a guide in the administration of fluids and diuretics. Vasodilator therapy of Nitroglycerine and Nitroprusside is to be started immediately, along with inotropes. If drug and medication therapy is not being tolerated, intra-aortic balloon counterpulsation or IABP must be taken into consideration. An immediate surgical closure is the treatment option of choice to improve surgical mortality.

Conclusion:

Postinfarction ventricular septal rupture refers to the rupture or tears in the ventricles of the heart after an initial episode of myocardial infarction or heart attack. There are several reasons for this condition, in addition to myocardial infarction. The clinical manifestation varies from patient to patient but is parallel to the etiological factors and underlying cardiovascular condition. Diagnosis is made via several measures and imaging modalities that are present, along with a good understanding of the patient's history. There are several treatment options that include medication therapy as well as invasive measures. Surgical intervention remains the standard gold of treatment management for postinfarction ventricular septal rupture.