Outpatient follow-up after cardiovascular interventions
Interventional cardiology is an emerging discipline with mature technology. A successful interventional technique is only the first step toward successful interventional treatment, and there is a great deal of follow-up work that needs to be done in the outpatient clinic. To ensure the final outcome of interventional patients, interventionalists must carefully follow up each patient who has undergone the operation with regular outpatient visits. Different interventional operations have different follow-up contents and requirements. According to the experience and requirements of the cardiology department of our hospital, different interventional operations are introduced as follows: Li Yibo, Department of Cardiology, Liaocheng People’s Hospital
Key points of follow-up and treatment after coronary intervention
I. Follow-up after coronary angiography
1. General clinical follow-up:
A. Follow-up and treatment of negative angiographic results.
a. Is the original symptom relieved or alleviated one week after discharge after inpatient examination and treatment? If yes, continue the treatment principle at the time of discharge. If no, the condition should be re-judged and the treatment medication should be adjusted. If necessary, ask for consultation of relevant disciplines.
b. Is there any new discomfort after discharge? If yes, make the necessary examination according to the specific situation, firstly, identify or exclude the late post-imaging complications, and make the necessary treatment.
B. Positive imaging results follow-up and management points.
a.Follow-up after PCI [see later].
b. Those with coronary atherosclerotic lesions but without indications for PCI.
Basic drug therapy.
(1), statin therapy. Emphasis on Ldh-c attainment.
(2), Aspirin therapy. Emphasize the mastery of counterindications.
(3), Intensive control of predisposing factors.
(4), Frequent health education is necessary.
2. One week postoperative puncture site examination.
A. Pay attention to the healing of the puncture site, observe whether there is blood oozing, redness and murmur, and whether there is any abnormality in the arterial pulsation, skin color, tension, temperature and activity of the punctured limb.
B. Check blood, urine routine, electrolytes, liver and kidney function, cardiac enzymes and infarction three.
C. If arteriovenous fistula, pseudoangioma or arteriovenous thrombosis is suspected, or if lumbar or abdominal pain or even anemia occurs via femoral artery puncture, corresponding vascular Doppler ultrasound examination should be performed and treated accordingly. For transflexion artery puncture, the forearm puncture site, forearm, upper arm and neck should be examined. Chest X-ray should be taken if there is abnormal chest tightness.
D. For suspected deep vein thrombosis, in addition to relevant venous ultrasound and D-dimer examination, ventilation ECT examination should be performed if necessary.
II. Follow-up and treatment after percutaneous coronary angioplasty (PCI)
1.The same as the follow-up after coronary angiography
2. Outpatient follow-up two weeks after PCI
a. To understand the tolerance of mandatory medications after PCI.
(1) Ask if there is any pain in the upper abdomen and lower back, black stools, muscle pain, etc.
(2). Find out if the patient has any digestive symptoms such as appetite.
(3). Check blood routine, blood sedimentation, liver function and kidney function.
b. Find out the effectiveness of mandatory medications after PCI: preferably within 1 month.
(1) Check blood lipids, blood glucose, etc.
(2). Check platelet aggregation rate. The inhibition rate of aspirin (AA) and clopidogrel (ADP) are required to be controlled between 40% and 70%, respectively. This is more important.
(3) The above indicators will be reviewed at least once more after 3 months.
3.Six-month PCI effectiveness evaluation:
(1), symptom inquiry: whether the symptoms completely disappeared before the intervention, if yes and no other discomfort then continue the medication. Doppler echocardiography, ambulatory electrocardiogram, and plate exercise tolerance test can be performed as appropriate. MR or exercise ECT is feasible for evaluation if necessary.
(2) If there is still or new chest pain, it is strongly recommended to review the platelet aggregation rate and also review the coronary multilayer spiral CT.
4. One-year PCI efficacy evaluation and decision making.
(1) For asymptomatic patients: perform a systematic physical examination, and also review ECG, Doppler echocardiography, liver function, kidney function, routine blood, urine, stool and occult blood, lipids and blood glucose. The rate of inhibition of platelet AAADP by aspirin and clopidogrel will be reviewed as a basis for later drug adjustment.
5.Ideas and strategies for the detection of recurrent myocardial ischemia after PCI
Recurrent myocardial ischemia after PCI may be the result of restenosis, the result of progression of the same or different coronary lesions, or the result of increased cardiac oxygen consumption due to various causes.
Typical clinical restenosis occurs about 3 months after PCI and reaches a plateau at 12 months. Occasionally, rapidly progressive restenosis occurs about 1 month after PCI, and angina that occurs after 12 months after PCI is more likely to be the result of progression of an existing atherosclerotic lesion or the development of a new lesion rather than restenosis. It is also important to note the presence of post-PCI chest pain caused by increased cardiac oxygen consumption, such as anemia and aortic valve stenosis. Increased mobility after peripheral arterial angioplasty in patients with intermittent claudication can also lead to increased myocardial oxygen consumption and chest pain.
Although asymptomatic restenosis occurs in approximately 10% of patients implanted with bare metal stents (BMS), there is no data to suggest that in these patients
routine post PCI loading test has a prognostic improvement. However, the American College of Cardiology (ACC)/American Heart Association (AHA) guidelines recommend that routine stress testing should be performed 3 to 6 months after PCI in patients at particular high risk (left heart insufficiency, multivessel disease, proximal left anterior descending lesions, history of sudden death, diabetes mellitus, hazardous occupations, and suboptimal PCI results). The physiological significance of clarifying other stenoses should also be taken into account before further PCI is performed. Exercise testing is not sensitive for restenosis diagnosis (its sensitivity is only 40% to 55%). Therefore, in patients with suspected restenosis, a more sensitive stress test combined with non-invasive myocardial imaging (nuclear myocardial perfusion, exercise echocardiography) should be performed. Routine angiographic review is required only in a few selective cases. These patients, including those with left main stem stenting, are to be reviewed with coronary angiography 3-9 months after the procedure.
6. Secondary prevention of coronary heart disease after PCI
(1) Control of risk factors
A large number of clinical trials have confirmed that active risk factor control for patients with definite CAD can improve survival, reduce recurrent cardiac events, and improve patients’ quality of life. For post-PCI patients with coronary artery disease, a comprehensive evaluation of their risk factors should be performed, and patients should be instructed to make lifestyle changes, combined with medications to control blood pressure, lipid and blood glucose levels. For patients who smoke, the goal is to quit completely and avoid smoking environments. For patients who continue to smoke, help establish a smoking cessation program and consider nicotine replacement drugs or bupropion if necessary.
treatment. Control blood pressure to below 140/90 mm Hg. For patients with diabetes or chronic kidney disease, hard control of blood pressure to below 130/80 mm Hg. Clinicians should recommend lifestyle modifications, including weight control, increased physical activity, reduced alcohol consumption, salt restriction, and increased intake of fresh vegetables, fruits, and low-fat diets. Patients whose blood pressure exceeds these targets should be given antihypertensive medication, with beta blockers and/or ACE inhibitors preferred, and if the target is still not met, the addition of thiazide diuretics may be considered. the target for lipid therapy in patients with CAD is a low-density lipoprotein (LDL-C) level of less than 100 mg/dL, and in high-risk patients it should be less than 70 mg/dL. if triglyceride (TG) levels exceed All patients should begin dietary therapy by reducing the intake of saturated fatty acids (no more than 7% of calories), trans fatty acids, and cholesterol (less than 200 mg/day). For TG levels between 200 and 499 mg/dL, add niacin or fenofibrate to control TG levels after LDL-C reduction therapy. If the TG level is 500 mg/dL or more, first apply fenofibrate or niacin to lower the TG level to prevent pancreatitis, and then continue statin LDL-C therapy after the TG level reaches the standard. Have 30 to 60 minutes of moderate to vigorous aerobic exercise (walking, jogging, swimming or cycling, etc.) exercise daily or at least 5 per week. Endurance exercise twice a week is encouraged. For post-PCI patients who have recently developed acute coronary syndrome or heart failure, an exercise program should be developed under physician supervision. Control body weight so that body mass index (BMI) is between 18.5 and 24.9 kg/m2 and waist circumference does not exceed 35 inches for women and 40 inches for men. If waist circumference exceeds these criteria, treatment of metabolic syndrome should be intensified. The starting goal is a 10% weight loss from baseline. Patients with diabetes whose target glycosylated hemoglobin level does not exceed 7% are encouraged to have lifestyle modification, medication, physical activity, and control of weight, blood pressure, and lipids.
(2) Secondary prevention drug therapy
To date, four classes of medications have been shown to reduce the incidence of cardiovascular events in patients with CAD: aspirin, beta-blockers, ACE inhibitors, and statin lipid-lowering agents. Overall the reduction in the risk of death from CAD is similar for all four classes of drugs, with a 25% to 30% reduction in risk, respectively, while the use of all four drugs together can benefit patients even more, with a 70% reduction in the overall risk of cardiovascular events.
(The role of antiplatelet therapy platelet activation in coronary atherosclerosis formation is no longer in doubt. In contrast, PCI treatment disrupts the integrity of the vascular endothelium, leading to exposure of the subendothelial matrix, which triggers platelet adhesion and aggregation, followed by the formation of platelet-rich thrombi, while activation of the coagulation system increases the size of the formed thrombi, resulting in lumen occlusion. The implantation of intracoronary stents can also activate platelets and increase the incidence of in-stent subacute thrombosis. Most in-stent thrombosis occurs early after stent implantation. With the current use of drug-eluting stents (DES), there is still a possibility of late in-stent thrombosis due to inhibition of intimal hyperplasia and poor endothelial coverage caused by the coated drug. In-stent thrombosis is a serious complication of PCI treatment, which is clinically uncommon but often causes myocardial infarction and sudden death. Anti-platelet agents can inhibit platelet adhesion aggregation and release functions and inhibit thrombus formation. Aspirin has become the standard of care in patients currently treated via PCI. A meta-analysis of the ATTC trial showed that in high-risk patients (including all post-PCI patients), the use of antiplatelet agents (mainly aspirin) reduced the combined endpoint of vascular death MI, or stroke, by nearly 25%. the M-HEARTII trial was a placebo-controlled study that enrolled 660 post-PCI patients. After successful PCI, patients were randomized to receive aspirin or placebo. 6 months later the incidence of postoperative infarction was significantly lower in the aspirin group. This study provides beneficial evidence for long-term aspirin use after PCI. Aspirin also reduced the incidence of ischemic events in patients with stable CAD, AMI or unstable angina after coronary angioplasty. Patients without aspirin resistance, allergy, or increased risk of bleeding should receive oral aspirin 325 mg daily for at least 1 month after BMS implantation, at least 3 months after rapamycin-coated stenting, and at least 6 months after paclitaxel-coated stenting, and 75 to 162 mg/day long-term thereafter.
Evidence for the effectiveness of long-term treatment with clopidogrel comes from the Clopidogrel Versus Aspirin in Patients at Risk for Ischemic Events (CAPRIE) trial . Patients were randomized to receive clopidogrel 75 mg/day or aspirin 75 mg/day to prevent recurrent vascular events. A total of 19,185 patients were enrolled and followed for 1-3 years, during which 617 new cases of MI occurred. MI occurred in 5.04% of patients in the aspirin-treated group and in only 4.2% of patients in the clopidogrel-treated group (p=0.008). 12,562 patients with acute coronary syndromes were studied in the CURE trial with clopidogrel. One year of clopidogrel treatment significantly reduced the incidence of CV death, MI or stroke compared with aspirin 75C325 mg/day. Further analysis of patients undergoing PCI in the CURE trial (PCI-CURE) confirmed the benefit of extended or combined clopidogrel and aspirin antiplatelet therapy after PCI, with a 31% reduction in the risk of death, MI, and the primary endpoint of stroke in patients at 9 months. Clopidogrel was administered at a loading dose of 300 mg before intervention and 75 mg daily thereafter. the long-term combination of clopidogrel with aspirin reduced the incidence of ischemic events. The course of clopidogrel is related to the interventional approach and the type of stent. In those with BMS implantation, clopidogrel 75 mg/day is applied for at least 1 month and at least 2 weeks if there is a risk of bleeding. Rapamycin-coated stents are applied for at least 3 months after surgery and paclitaxel-coated stents for at least 6 months after surgery, and up to 12 months if there is no risk of bleeding. In contrast, long-term administration of clopidogrel 75 mg/day is recommended in patients receiving vascular radiation therapy if there is no risk of bleeding. Clopidogrel can also be used in patients who are intolerant to aspirin due to ulcerative bleeding.
Oral anticoagulation with warfarin after PCI, even in combination with aspirin, is less effective than dual antiplatelet therapy in preventing acute in-stent thrombosis. On the other hand, warfarin is necessary in certain patients, such as those with combined valvular heart disease or chronic atrial fibrillation. In patients with combined atrial fibrillation or other indications for warfarin, the optimal dose of the drug after PCI should be individualized, weighing the risk of embolization and stent thrombosis against the risk of bleeding complications after dual antiplatelet therapy plus warfarin.
( Lipid-modifying therapy A large body of medical research evidence suggests an etiologic causal relationship between dyslipidemia and the onset and progression of atherosclerotic disease. Patients undergoing PCI are at risk for both the presence of multiple plaques in the coronary arteries and failure to undergo complete interventional intervention. Moreover, PCI is a purely mechanical treatment, and its compression of the plaque triggers numerous pathophysiological reactions, both necessary for vascular tissue repair and harmful to the organism and the local vasculature. Even though the newly introduced and widely used pharmacological stent therapy has a partial etiologic effect, its effectiveness is still very limited. Clinical studies have confirmed that the incidence of cardiovascular events in patients with CAD is higher than normal even after complete revascularization, and that aggressive adjuvant therapy such as lipid-modifying antithrombotic therapy can significantly reduce the incidence of cardiovascular events. Statins are the first choice of lipid-regulating therapy after PCI. The LIPS (Lysaght Interventional Prevention Study) was conducted in 1677 patients who underwent first-time successful PCI (with or without stent placement). randomized to receive fluvastatin 80 mg/day or placebo for 3 to 4 years. The results showed that fluvastatin significantly reduced the incidence of major adverse cardiovascular events by 22% (p=0.01). statin therapy in CAD patients after PCI reduced the incidence of in-stent restenosis. the REGRESS trial looked at the 2-year outcomes of 201 CAD patients treated with pravastatin 40 mg/day or placebo after PCI and found that the incidence of restenosis was higher in the pravastatin 40 mg/day and placebo groups were 7% and 29%, respectively, with a 58% reduction in all cardiovascular events in the pravastatin group.Walter DH et al. retrospectively analyzed 525 post-PCI patients, 258 of whom were on statin and 267 of whom were not on statin. The restenosis rates were 25.5% and 38% at 6 months after stenting (P<0.005
Patients with coronary artery disease after PCI are considered high-risk patients according to the ATPIII guidelines and should have a lipid-modifying therapy goal of an LDL-C level below 100 mg/dL. after an acute event, they should be considered very high-risk patients and have a lipid-modifying therapy goal of an LDL-C level below 70 mg/dL. statin therapy after coronary artery disease PCI is a long-term treatment: there is evidence that abrupt discontinuation of statin therapy in patients with coronary artery disease can lead to an increase in cardiovascular events by an unknown mechanism. Recent studies have confirmed that after 6 weeks of statin therapy, inflammatory factors in the blood of patients on the third day of abrupt discontinuation showed a significant rebound, suggesting that statin is a long-term therapeutic decision. In addition, most post-PCI patients with coronary artery disease are elderly and often have multiple coexisting conditions that require multiple medications, at which point, attention should be paid to drug interactions and safety.
(ACE inhibitors A large body of evidence-based medical evidence confirms that ACE inhibitor (ACEI) therapy improves the long-term prognosis, reduces death, and delays the progression of heart failure in patients with AMI as well as post-myocardial infarction cardiac dysfunction or heart failure. the HOPE trial confirmed that ACEI therapy is effective in reducing cardiovascular morbidity and mortality in all patients at high risk for CAD. Therefore, the 2002 update of the ACC/AHA guidelines for the treatment of chronic stable angina recommended that all patients with CAD should receive ACEI therapy, thus extending the indication for ACEI in CAD from post-MI patients to all patients with high-risk CAD. The EUROPA study showed that in patients with stable CAD, perindopril 8 mg/d for 4 years significantly reduced the incidence of endpoint events such as MI, stroke, and cardiac death, thus significantly improving the prognosis of patients with CAD, and this improvement in long-term prognosis was obtained on top of already receiving antiplatelet agents, beta-blockers, and statins, beyond their antihypertensive beyond their antihypertensive effects. Patients who are intolerant to ACEIs may opt for angiotensin II receptor antagonists
(ARBs). Randomized controlled trials (RCTs) have shown that the benefits of ACEI therapy extend beyond those in patients with AMI, heart failure, and severe cardiac dysfunction. In the Angiotensin-Converting Enzyme Inhibitor Post-Angioplasty Study (APRES), ACEI ramipril reduced the incidence of cardiac death, AMI, and heart failure and improved cardiac function in patients without recent MI, without clinical evidence of heart failure, after coronary artery bypass grafting, and in patients treated with PCI. Application of ACEI to try to achieve the target dose in the trial was necessary to obtain significant efficacy.
( The use of beta-blockers after coronary PCI beta-blockers are well documented as secondary prevention of CAD, reducing the incidence of all-cause death, CV death, recurrent nonfatal MI, and sudden death. In direct PCI, beta-blocker use (intravenous metoprolol) has been shown to benefit by reducing malignant arrhythmias and reducing periprocedural CK-MB release, improving left ventricular function at 30 days of follow-up. A meta-analysis of the Post-MI Direct Angioplasty (PAMI) trial, PAMI-2, and the Stent-PAMI trial enrolled 2537 patients who underwent direct angioplasty after acute MI. The effect of intraoperative beta-blocker pretreatment during PCI on the clinical profile, angiographic and prognostic outcomes of patients was investigated. After correction for baseline differences, in-hospital mortality was significantly lower (p < 0.0148) and one-year mortality was lower (p = 0.11) in patients with beta blocker application. In another randomized, placebo-controlled trial enrolling 150 patients undergoing conventional PCI, intravenous application of probenecid 15 g/kg significantly reduced troponin T and CK-MB levels. The association of beta-blockers with coronary restenosis has also been studied. In vitro studies have shown that carvedilol directly inhibits vascular smooth muscle cell migration and proliferation by inhibiting mitogen-activated protein kinase activity and by regulating the cell cycle. In carotid angioplasty rats, carvedilol inhibited neoplastic endothelial proliferation by 84% through its action on growth factors. In human clinical studies, a prospective trial investigated the use of beta-blockers in patients after PCI. The trial enrolled 4840 post-PCI patients. The primary endpoint was the incidence of clinical restenosis at 6 months. the incidence of clinical restenosis was 10.0% in the β-blocker group, which was significantly lower than in the control group (13.5%, P=.004). However, some clinical trials have also concluded to the contrary that β-blockers do not have a preventive effect on coronary restenosis. However, β-blockers should be used to improve prognosis in all patients with CAD diagnosed with MI, acute coronary syndrome, or left ventricular insufficiency, in the absence of contraindications. In patients with a diagnosis of coronary artery disease, or diabetes mellitus, long-term beta-blocker therapy should also be used unless contraindicated.