Secondary prevention of coronary heart disease and basics of stroke: the value of lipid-lowering therapy and the identification of ischemic and hemorrhagic stroke

39. Precautions and Influencing Factors When Taking Warfarin: Cefazolin inhibits the production of vitamin K in the intestines, reducing vitamin K absorption and hindering the synthesis of clotting factors; cimetidine and metronidazole inhibit warfarin metabolism; cholestyramine binds to warfarin in the intestines, reducing its absorption and bioavailability; barbiturates, rifampin, and griseofulvin accelerate warfarin metabolism. Furthermore, warfarin is completely absorbed orally and almost entirely bound to plasma proteins after entering the bloodstream. Therefore, patients are more sensitive to warfarin when plasma protein levels are low, such as during acute illnesses or after surgery.

40. How to use lipid-lowering drugs to treat angina pectoris. Patients with angina pectoris due to coronary heart disease should use lipid-lowering drugs regardless of whether they have hyperlipidemia, as lipid-lowering treatment helps reduce or eliminate coronary atherosclerotic plaques. Statins, specifically HMG-CoA reductase inhibitors, are mainly used. HMG-CoA reductase is the rate-limiting enzyme in cholesterol synthesis; HMG-CoA reductase inhibitors inhibit the synthesis of HMG-CoA reductase, thereby reducing cholesterol synthesis. Adverse reactions include fatigue, myalgia, gastrointestinal symptoms, rash, and abnormal liver and kidney function. Commonly used drugs include: simvastatin (Zocor), pravastatin (Praclostrobin), fluvastatin (Lescol), and atorvastatin (Lipitor).

41. What are the main adverse reactions of various drugs for treating coronary heart disease? (1) Nitrates: Headache, facial flushing, dizziness, palpitations, and occasionally, a drop in blood pressure. (2) Beta-blockers: Bradycardia, orthostatic hypotension, induction of heart failure, and induction of bronchial asthma. (3) Calcium channel blockers: Dizziness, fatigue, insomnia, constipation, bradycardia (e.g., verapamil) or tachycardia (e.g., nifedipine), and lower extremity edema. (4) Antiplatelet drugs: Gastrointestinal irritation and bleeding tendency. (5) Lipid-lowering drugs: Liver damage and, occasionally, rhabdomyolysis.

42. Which types of medications for treating coronary heart disease require long-term use? For patients with coronary heart disease, it is recommended that, if well tolerated, they take beta-blockers, angiotensin-converting enzyme inhibitors, antiplatelet drugs, and lipid-lowering drugs long-term. Long-term use of these medications can significantly reduce the mortality rate of cardiovascular disease patients.

43. What is Secondary Prevention of Coronary Artery Disease (CAD)? Secondary prevention of CAD refers to the active treatment of patients already diagnosed with CAD to prevent disease progression and strive for its reversal. The "ABC" approach is widely recognized as the three major therapies for modern treatment and secondary prevention of CAD. These are: A: Aspirin; B: Beta-blockers; C: Lipid-lowering therapy. Generally, low-density lipoprotein cholesterol (LDL-C), hypertension, and smoking are considered key aspects of secondary prevention, and stronger preventative measures should be taken against these important risk factors. In summary, this includes adopting a diet that lowers lipid levels and blood pressure; reducing weight; achieving optimal diabetes treatment; achieving optimal blood pressure and lipid control; quitting smoking; and maintaining regular physical activity and exercise. CAD not only causes pain and discomfort but also affects cardiac function, reducing the patient's ability to perform physical activities. Decreased cardiac function means reduced work capacity. Protecting cardiac function is also one of the purposes of some medications we take.

Section 4 Stroke 1. What is a Stroke? A stroke, commonly known as apoplexy, is an acute disruption of cerebral blood circulation that occurs suddenly on the basis of diseases such as hypertension and cerebral arteriosclerosis, leading to acute cerebral dysfunction. Its main clinical manifestations include headache, dizziness, and altered consciousness. Severe cases may present with hemiplegia, decreased sensation on one side of the body, and speech impairment. Because cerebrovascular diseases have a rapid onset, change rapidly, and manifest in various ways, they share similarities with the characteristics of wind in nature-starting in an instant, changing abruptly, and unpredictably-hence the name "stroke."

2. What are the different types of stroke? Stroke can be broadly classified into two categories: ischemic stroke and hemorrhagic stroke. (1) Ischemic stroke: The cause of ischemia can be the formation of thrombi in cerebral blood vessels, which obstructs the blood supply to the brain tissue; or it can be that emboli in the blood block blood vessels of the corresponding diameter during the flow, causing local cerebral ischemia. The former is called cerebral thrombosis, and the latter is called cerebral embolism. There is also a type of transient ischemic attack caused by cerebral vasospasm, the detachment of microemboli in arteries, and compression of arteries by surrounding tissues. All three types of attacks cause ischemic cerebrovascular disease. (2) Hemorrhagic stroke: One type is caused by the rupture of blood vessels in the brain, which bleeds into the brain and forms a hematoma, called cerebral hemorrhage; the other type is caused by the rupture of blood vessels in the superficial part of the brain, which allows blood to enter the subarachnoid space, called subarachnoid hemorrhage.

3. What is Cerebral Infarction? Cerebral embolism commonly occurs in young adults, and patients often have underlying diseases that can produce emboli, such as rheumatic heart disease, congenital heart disease, or other conditions. Its characteristics include: rapid onset, often occurring during activity, with symptoms reaching their peak within minutes to seconds; it is the fastest-onset of all cerebrovascular diseases. Cerebral thrombosis is common in the elderly, and patients often have cerebral arteriosclerosis, hypertension, hyperlipidemia, etc. Its onset is slow, often occurring during rest or sleep, and typically reaching its peak within 1-3 days. Seizures are rare, and hemiplegia often gradually worsens. Because the infarction originates from thrombosis in the cerebral arteries themselves, symptom improvement is relatively slow. Lacunar infarction is a special type of microinfarction caused by hyaline degeneration of small arteries due to long-term chronic hypertension; some cases are due to microembolism caused by arteriosclerosis. The diameter of the infarct lesion is generally 0.2-15 mm. After the necrotic and softened tissue is phagocytosed and removed, small cystic cavities may remain, hence the name lacunar infarction. This disease can recur, and when lacunar infarction occurs, it is called lacunar state. The incidence rate is approximately 20%–30% of all cerebral infarctions.

4. What is a Transient Ischemic Attack (TIA)? A transient ischemic attack (TIA), commonly known as a mini-stroke, refers to a brain dysfunction caused by paroxysmal cerebral ischemia. It commonly occurs in middle-aged and elderly people, and most patients have hypertension, hyperlipidemia, diabetes, and heart disease. The onset of symptoms usually lasts for several minutes, but no longer than 24 hours, and tends to recur and subside. Its clinical characteristics include acute onset, often occurring while the patient is conscious, with each attack presenting with the same symptoms. Symptoms and signs reach their peak within seconds, causing neurological dysfunction in the corresponding area, such as contralateral upper and lower limb or unilateral limb paralysis, mild sensory loss or paresthesia, aphasia, and sometimes unilateral visual impairment due to ophthalmic artery ischemia, or dizziness, nausea, vomiting, hemianopsia or double vision, gait instability, dysphagia, sensory and motor disturbances. It can affect the face and limbs, and some patients may experience falls due to sudden loss of consciousness. It generally lasts for a few seconds or minutes, but can also last for several hours, but no longer than 24 hours, and has no sequelae. Transient ischemic attacks (TIAs) can occur several times a day, even dozens of times, or once every few days, or even occasionally. Multiple TIAs within a short period are often a sign of a serious stroke. Timely diagnosis and treatment of TIAs are crucial for preventing stroke.

5. What is Cerebral Hemorrhage? Cerebral hemorrhage, also known as intracerebral hemorrhage, refers to intracranial bleeding caused by lesions in the cerebral blood vessels themselves. Hypertension and arteriosclerosis are the main causes, and some patients have a history of cerebrovascular disease or diabetes. Other common causes include cerebral vascular malformations, intracranial aneurysms, blood diseases, intracranial tumors, intracranial inflammation, and trauma. About 80% of patients have very high blood pressure some time before the onset of the disease. Cerebral hemorrhage accounts for 20%–30% of acute cerebrovascular diseases and 40% of hemorrhagic cerebrovascular diseases, with a mortality rate of 40%, the highest among acute cerebrovascular diseases. The onset of cerebral hemorrhage is generally rapid, with severe clinical manifestations appearing quickly, usually reaching their peak within one to several hours. Clinical manifestations depend on the amount and location of the bleeding. Patients with moderate to large hemorrhages often suddenly experience dizziness, headache, vomiting, altered consciousness, hemiplegia, aphasia, and urinary and fecal incontinence, followed by coma within minutes. Slower-progressing hemorrhages are characterized by small, recurrent, or prolonged bleeding. CT scans can be used for diagnosis. During a cerebral hemorrhage, there is often a significant increase in blood pressure, frequently exceeding 200/120 mmHg, and in some patients reaching around 250/150 mmHg or even higher. This severe increase in blood pressure is related not only to pre-existing hypertension but also to increased intracranial pressure after the hemorrhage and the patient's agitation, and it is often difficult to lower. Patients with this particularly high blood pressure often experience progressive disease deterioration and have a poor prognosis.