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Tang Li
Cardiology
About me
Beijing Boai Hospital, Cardiovascular Department, attending physician, has been engaged in clinical work in cardiac internal medicine for many years, with rich clinical experience in the diagnosis and treatment of cardiovascular diseases.
Proficient in diseases
Specializes in the diagnosis of common cardiovascular diseases such as coronary heart disease, hypertension, arrhythmia, atrial fibrillation, paroxysmal supraventricular tachycardia, heart failure, myocarditis, congenital heart disease, cardiomyopathy, and atrial septal defect.
Voices
Can atrial fibrillation cause cerebral infarction?
Patients with chronic atrial fibrillation have a relatively high incidence rate of embolism. For instance, those with a history of embolism, valvular disease, hypertension, diabetes, elderly patients, left atrial enlargement, and coronary artery disease are at increased risk of embolism. Atrial fibrillation is an independent risk factor for stroke. As age increases, the incidence of stroke in patients with atrial fibrillation also increases annually; atrial fibrillation doubles the mortality rate of stroke and significantly increases the disability rate. At the same time, atrial fibrillation also significantly increases the risk of recurrent stroke. Studies show that the incidence of stroke within the first year after a stroke is 6.92% in patients with atrial fibrillation, compared to 4.7% in those without atrial fibrillation. Therefore, anticoagulation therapy is the primary strategy for managing atrial fibrillation.
Can someone with an atrial septal defect get pregnant?
Whether patients with atrial septal defects can become pregnant depends on the following factors: 1. Whether the patient normally has symptoms. 2. Whether the echocardiography indicates heart enlargement or pulmonary hypertension. 3. The size of the atrial septal defect. 4. Whether there is a combination of arrhythmias such as atrial flutter or atrial fibrillation, and complications such as pulmonary hypertension or heart failure. For those without symptoms, and where the defect does not cause pulmonary hypertension or right heart enlargement, choosing to become pregnant is possible. Complications are not common in pregnant women with isolated atrial septal defects without pulmonary hypertension. Studies have shown that the incidence of complications in pregnant women, whether the defect is repaired or not, is relatively low. If the patient has related arrhythmias and complications, it should be closely monitored, because the cardiovascular system of the mother undergoes changes during pregnancy, leading to increased cardiac workload and a higher burden on the heart, which in turn can increase the incidence of arrhythmias. For women who are already at high risk of atrial flutter or fibrillation, this risk can increase further. Additionally, pregnant women are in an older physiological state, making it easier to form blood clots, and for those with atrial septal defects, the risk of paradoxical thrombosis increases.
What are the symptoms of bradycardia?
The normal heart rate for an adult is between 60-140 beats per minute. If it falls below 60 beats per minute, it is generally referred to as bradycardia. Most patients with bradycardia may not have symptoms, but those who do should be closely monitored. The symptoms of bradycardia mainly arise from a reduced cardiac output, leading to insufficient blood supply to the heart and brain, thereby causing symptoms. Patients may experience dizziness, fatigue, poor mental performance, and other symptoms. Some patients may experience dizziness, transient blackouts before the eyes, fatigue, palpitations, chest tightness, and shortness of breath. In severe cases, patients may also experience fainting.
Is hyperlipidemia fatty liver disease?
Hyperlipidemia and fatty liver are actually two different concepts. Hyperlipidemia is essentially dyslipidemia, which refers to abnormal quality and quantity of lipids in the plasma. The tests for blood lipids include total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. With our medical history, physical signs, and laboratory tests, diagnosing hyperlipidemia is not difficult. The current diagnostic criteria are mainly based on the 2017 Chinese guidelines for the prevention and treatment of dyslipidemia in adults, where low-density lipoprotein greater than 4.14 mmol/L suggests elevated low-density lipoprotein. Fatty liver, on the other hand, refers to excessive fat accumulation within liver cells due to various reasons, and is a common pathological change in the liver, rather than an independent disease. Patients with hyperlipidemia are prone to fatty liver.
Causes of arteriosclerosis
The etiology of arteriosclerosis has not been fully determined, and studies indicate that arteriosclerosis is a multifactorial disease, caused by multiple factors acting at different stages, which are referred to as risk factors. The primary risk factors include the following: First, age and gender. Clinically, it is more common in middle-aged and elderly people over forty years old. After the age of forty-nine, the progression is fast, but early arteriosclerotic changes have also been found in autopsy of some young adults and even children. In recent years, clinical onset age tends to be younger. Compared to men, the incidence rate in women is lower, because estrogen has a protective effect against arteriosclerosis. Therefore, the incidence rate in women increases rapidly after menopause. Age and gender are unchangeable risk factors. Second, abnormal lipid levels, with abnormal lipid metabolism being the most important risk factor for arteriosclerosis. Third, hypertension, as the incidence of arteriosclerosis in patients with hypertension is significantly higher. Sixty to seventy percent of patients with coronary arteriosclerosis have hypertension, and patients with hypertension are three to four times more likely to have arteriosclerosis compared to those with normal blood pressure. Fourth, smoking, as the incidence and mortality rate of coronary arteriosclerosis in smokers are two to six times higher than in non-smokers, and it correlates positively with the number of cigarettes smoked daily. Secondhand smoke is also a risk factor. Fifth, diabetes and glucose intolerance, where not only is the incidence of arteriosclerosis in diabetic patients several times higher than in non-diabetics, but the progression of the disease is also rapid. Sixth, obesity, defined as being more than twenty percent over the standard weight or a BMI greater than twenty-four. Obesity is also a risk factor for arteriosclerosis. Seventh, family history, where a family history of coronary heart disease, diabetes, hypertension, and hyperlipidemia significantly increases the incidence of coronary heart disease. Various theories have been proposed to explain the pathogenesis of coronary arteriosclerosis from different perspectives. These include the lipid infiltration theory, thrombosis theory, and smooth muscle cell clonal theory. In recent years, the endothelial damage response theory has gained more support, suggesting that the disease results from various risk factors ultimately damaging the arterial intima, and the formation of arteriosclerosis lesions is an inflammatory, fibro-proliferative response of the arteries to endothelial damage.
Treatment of Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy, due to unknown causes and often related to genetic factors, is difficult to prevent. It is important to guide patients on how to lead their lives, reminding them to avoid intense physical activities, heavy lifting, or breath-holding to reduce the incidence of sudden death. Avoid using drugs that enhance myocardial contractility and reduce cardiac capacity load, such as digoxin and nitrates, to decrease the aggravation of left ventricular outflow tract obstruction. The treatment principle for this disease is to slow down the hypertrophy of the myocardium, prevent tachycardia, and maintain normal sinus rhythm. It also aims to relieve the narrowing of the left ventricular outflow tract and counteract arrhythmias. Currently, the use of beta blockers and calcium channel blockers is advocated. For severe obstructive patients, interventional and surgical treatments can be carried out, including the implantation of a dual-chamber DTD pacemaker, and the ablation or removal of hypertrophied interventricular septum myocardium.
What are the clinical considerations for acute pericarditis?
The treatment and prognosis of acute pericarditis mainly depend on the cause, and are also related to whether it is diagnosed and treated correctly early on. For various types of pericarditis, if constrictive syndrome occurs, pericardiocentesis should be performed immediately to relieve symptoms. In cases like tuberculous pericarditis, if not treated aggressively, it can usually progress to chronic constrictive pericarditis. Acute nonspecific pericarditis and post-cardiac injury syndrome may lead to recurrent attacks of pericarditis after the initial episode, known as recurrent pericarditis, with an incidence rate of about 20%-30%. This is one of the most difficult complications of acute pericarditis to manage. Clinically, it generally presents similar to acute pericarditis, with recurrent attacks months or years after the initial episode, accompanied by severe chest pain. Most patients should be treated again with high doses of non-steroidal anti-inflammatory drugs, slowly tapering over several months until the medication can be stopped. If ineffective, corticosteroid treatment may be administered; in severe cases, intravenous methylprednisolone may be given, and symptoms in most patients may improve within a few days. However, it is important to note that symptoms often reappear during steroid tapering.
Is moderate pulmonary hypertension serious?
Pulmonary hypertension is a common clinical condition with complex etiology, which can be caused by various cardiac, pulmonary, or pulmonary vascular diseases. The current diagnostic criteria for pulmonary hypertension are an average pulmonary arterial pressure greater than 25 mmHg at sea level in a resting state, or greater than 30 mmHg during exercise, as measured via right heart catheterization. The severity of pulmonary hypertension can be categorized based on resting average pulmonary arterial pressure levels into mild (26 to 35 mmHg), moderate (36 to 45 mmHg), and severe (greater than 45 mmHg). Echocardiography is the most important non-invasive screening method for pulmonary hypertension. Assessing the severity of moderate pulmonary hypertension not only involves the measurement of average pulmonary arterial pressure but also necessitates identifying its etiology. Since pulmonary hypertension is a disease with a complex etiology, it is crucial to first clarify the cause, and then further determine the patient's cardiopulmonary function status, whether it is in a compensatory or decompensatory stage. Additionally, it is important to determine if there are any related complications, such as pulmonary hypertension stemming from lung-induced conditions. When patients exhibit complications like pulmonary encephalopathy, acid-base imbalance, electrolyte disturbances, arrhythmias, or even shock and gastrointestinal bleeding, the severity of pulmonary hypertension can be extremely severe.
Can atrial septal defect be cured?
Atrial septal defect is a common congenital heart disease. When the defect is small, some patients may heal naturally. In recent years, with the development of interventional technology for congenital heart diseases, most patients with atrial septal defects can be completely cured through interventional treatment, and some through surgical treatment. However, some patients have a large atrial septal defect with significant left-to-right shunting, leading to severe pulmonary arterial hypertension and right heart failure, which generally results in a poor prognosis. Some patients also have complications such as atrial flutter and atrial fibrillation. Certain patients may experience right heart failure due to excessive load on the right ventricle, and these patients often have a poor prognosis.
What are the symptoms of patent ductus arteriosus?
Patients with patent ductus arteriosus may exhibit several clinical manifestations based on the amount of shunting. 1. Small shunt volume: The internal diameter of the patent ductus arteriosus is small, and the patient may exhibit no subjective symptoms. The prominent sign is a continuous machinery murmur heard at the left sternal border at the second intercostal space and below the left clavicle, accompanied by a thrill; pulse pressure may slightly increase. 2. Moderate shunt: Patients commonly experience fatigue, palpitations, shortness of breath, and chest discomfort after exertion. The heart murmur is similar in character to the above but louder, accompanied by a thrill, and widely transmitted. At times, diastolic and mild systolic murmurs caused by left ventricular enlargement, relative mitral valve insufficiency, and stenosis can be heard at the apex, with a positive vascular sign. 3. Large shunt volume: This condition in a patent ductus arteriosus often accompanies secondary severe pulmonary hypertension, leading to a right-to-left shunt. The typical murmur's diastolic component may diminish or disappear, followed by the disappearance of the systolic murmur, and only a diastolic murmur due to pulmonic valve insufficiency can be heard. Patients often exhibit cyanosis and severe clinical symptoms.