Definition of metabolic syndrome
2007
1.Abdominal obesity: waist circumference >90cm for men and >85cm for women.
2.TG≥1,7mmol/L.
3, HDL-C <1, 04mmol/L.
4, blood pressure ≥130/85mmHg.
5, fasting blood glucose ≥6, 1mmol/L, 2 hours postprandial blood glucose ≥7, 8mmol/L or history of diabetes mellitus.
Pathological basis of metabolic syndrome
In 1988, Reaven found that obesity, type 2 diabetes, abnormal lipid metabolism, hypertension, hyperinsulinemia and coronary heart disease often occurred in the same patient, and called this phenomenon “X syndrome”. 1999, the World Health Organization named this series of clinical manifestations as “Metabolic syndrome”.
Since then, many international organizations have discussed metabolic syndrome, but the definition of metabolic syndrome varies, and there is even a debate on whether the phenomenon exists. Metabolic syndrome is a group of clinical manifestations based on the pathophysiology of insulin resistance and includes multiple risk factors, including central obesity, elevated blood pressure, abnormal glucose and lipid metabolism, hyperinsulinemia, procoagulant state, increased urinary protein excretion, endothelial dysfunction, hyperuricemia, and increased levels of inflammatory markers.
Clinical manifestations of metabolic syndrome
It is easy to find that the core clinical manifestations of metabolic syndrome are “three highs and one abnormality”, i.e. high body weight, high blood pressure, high blood sugar and abnormal lipid metabolism, after taking a closer look at the definition of metabolic syndrome in domestic and international guidelines.
Since metabolic syndrome is a syndrome, it is not a unique disease, and there is no need to argue whether it exists or not, as long as the clinical manifestations meet the common features mentioned above, it can be diagnosed as metabolic syndrome. Other clinical manifestations of metabolic syndrome include homocysteinemia, elevated uric acid, procoagulant state, abnormal alpha lipoprotein, fibrinogen and fibrinogen activator inhibitor-1 levels. Patients with metabolic syndrome are actually high-risk patients with multiple risk factors for cardiovascular disease. “Premature ventricular contractions, one of the most common arrhythmias, are the most common form of ventricular contractions. The incidence of ventricular premature beats is the most common arrhythmia in China and worldwide. Many ventricular premature contractions occur in healthy individuals, and the detection rate of ventricular premature contractions is as high as 70-90% in the general population and is also common in patients with organic heart disease.
Premature ventricular contractions are abnormal electrical excitations originating in the ventricular myocardium or in the Purkinje fibers of the ventricular myocardium in advance. Ventricular premature contractions may occur singly or in pairs, or even in series of 3-5 contractions, and may occur occasionally or frequently. In general, the incidence and complexity of premature ventricular contractions increase with age, and the number of premature ventricular contractions also has a circadian rhythm, with sympathetic excitability being higher at all these stages. In addition, most functional ventricular prematureness decreases after exercise, while pathological ventricular prematureness is new or increases in number after exercise.
Recognizing the natural variability of ventricular prematureness and evaluating ambulatory ECG reports
The natural variability of ventricular prematureness, in which ventricular prematureness at different times can increase or decrease by 70% under natural circumstances, is known as the natural variability of ventricular prematureness. Understanding this characteristic of ventricular prematureness helps to reduce the blindness of excessive pessimism or optimism, and the natural variability of ventricular prematureness should also be taken into account when judging the efficacy of antiarrhythmic drugs, which are considered effective only if they reduce the total number of ventricular prematureness by 70% or more, while natural reduction cannot be excluded for changes of less than 70%.
There is no unanimous opinion on the evaluation of normal or abnormal number of ventricular premature in the ECG report. Most of the literature considers that the total number of ventricular premature is ≤100/24 hours when normal and >100/24 hours as frequent ventricular premature, while others suggest that intervention should be started when the total number of ventricular premature is ≥10% of the total heart rate throughout the day. In fact, the total number of ventricular premature reported by ECG is only a reference indicator and has no independent significance in determining the prognosis, which must be considered in conjunction with clinical considerations.
Correct treatment of ventricular premature RonT phenomenon
Theoretically and practically, it has been confirmed that ventricular fibrillation is often induced by ventricular prematureness on the T wave of the electrocardiogram, and RonT ventricular prematureness is classified into type I and type II according to the absence or prolongation of the QT interval. Because of the risk of ventricular fibrillation, clinicians are at risk when they encounter RonT ventricular premature.
The correct evaluation of RonT ventricular premature is crucial, and it should be clear that the incidence of this type of ventricular premature is low, accounting for only 2% of all ventricular premature events in the 24 hours before acute myocardial infarction. In addition, not all RonT premature ventricles can trigger ventricular tachycardia and ventricular fibrillation. 8% of RonT premature ventricles occur within 10 minutes after the onset of acute coronary syndrome, but only 4% of ventricular tachycardia or ventricular fibrillation is triggered by RonT premature ventricles during this period. whether RonT premature ventricles can trigger ventricular tachycardia and ventricular fibrillation is related to a variety of factors, especially the underlying cardiac status, sympathetic nerve activity, and the patient’s threshold for ventricular fibrillation. Therefore, RonT ventricular premature should be highly valued and objectively evaluated, but should never be overly feared and subsequently overtreated.
Functional ventricular dysfunction – no treatment required
Functional ventricular prematureness is defined as ventricular prematureness in patients without organic heart disease, who may have abnormal autonomic function, especially increased sympathetic excitability.
The characteristics of functional ventricular premature are as follows.
1, mostly in young people, while ventricular prematureness in the elderly or children often has a cause.
2, episodes are often accompanied by elevated sympathetic excitation or have excitatory triggers.
3, the onset of complaints are many and bizarre and dramatic, on the contrary, without any complaints and found in the physical examination of ventricular premature is mostly pathological.
4, poor efficacy of antiarrhythmic drugs.
5, electrocardiogram without atrioventricular or intraventricular block and without abnormalities such as left ventricular hypertrophy.
6, the QRS wave amplitude of ECG ventricular premature is high and the time limit is short, on the contrary, the morphology of pathological ventricular premature is often stumpy, that is, the QRS wave is wide and low. Functional ventricular premature is not accompanied by hemodynamic changes and is a benign ventricular arrhythmia, so no treatment is needed.
Ventricular prematureness after myocarditis – do not overtreat
Currently, overtreatment of post-ventricular premature viral myocarditis is a common phenomenon, which is manifested by the prolonged duration of antiarrhythmic drug treatment (>6 months), and children are even required to be exempted from physical education classes or suspended from school, which is not only unhelpful to treatment, but also increases the mental burden of the child and even causes psychological disorders.
Viral myocarditis is clinically common, occurring in about 4% of patients per influenza. Although fulminant viral myocarditis is a serious and dangerous disease, it is only seen in a very small number of patients, and the majority of patients have a mild or even asymptomatic disease that has resolved itself. About 90% of patients may develop various arrhythmias, with ventricular prematureness being the most common.
In the treatment of ventricular prematureness in patients with viral myocarditis, a small number of patients with severe symptoms may be treated with targeted medications, which should be continued for 2 to 3 months after the symptoms disappear, followed by an ambulatory electrocardiogram to determine the next step in treatment. When the patient still has complex ventricular prematureness, treatment must be continued for 2 to 3 months. In general, antiarrhythmic drug therapy is no longer administered after 6 months of the acute phase, because overtreatment is detrimental, and ventricular prematureness in patients at this time is associated with scarring from local inflammation and is not related to long-term prognosis, neither affecting normal life and work nor fatal arrhythmias.
Some pathologic ventricular prematureness requires only cause-specific treatment
Pathological ventricular prematureness in young people is mostly seen in patients with viral or rheumatic myocarditis, and in elderly people with combined coronary artery disease, hypertension or heart failure. Even when the number of pathological ventricular premature is high, even with symptoms, there is no need for antiarrhythmic drug treatment for ventricular premature, but should take corresponding measures for the cause, such as improving cardiac function, lowering blood pressure, crown expansion, improving myocardial blood supply and other causal treatment for the original disease.
Some of the ventricular premature that deserve high priority
While emphasizing that most ventricular premature events are benign arrhythmias, it does not mean that all ventricular premature events can be ignored. There is considerable evidence that the prognosis of cardiac patients is related to the number and complexity of ventricular premature events. Clinicians should pay attention to “complex ventricular premature”, i.e., patients with organic heart disease who present with ECG abnormalities in addition to ventricular premature.
The following conditions should also be taken into account when patients with ventricular prematureness are present.
1, there are clinical manifestations such as vertigo, black haze or aura syncope, etc.
2. organic heart disease.
3. The presence of structural and functional changes in the heart.
4.History of hereditary arrhythmias or family history.
5, the presence of multi-source, paired and serial ventricular premature on ECG, as well as the presence of RonT ventricular premature on the basis of acute infarction or QT prolongation.
Pharmacological treatment strategy for ventricular drought
If the patient has palpitations, especially if the symptoms are frequent and have affected quality of life or hemodynamics, pharmacological treatment may be given to improve quality of life. However, the removal of possible irritants, such as tobacco, caffeine, stress, anxiety, and other potential risk factors for antiarrhythmic drugs, must be considered first.
If symptoms persist, moderate anxiolytics or beta-blockers can be used. beta-blockers are safer for treating both the symptoms and the cause of the arrhythmia, although they are moderately effective in controlling ventricular prematureness and have minimal arrhythmogenic effects. The Ι class of antiarrhythmics, such as mexiletine, propafenone hydrochloride, morethizine, and amiodarone, are rarely used because of their many side effects. Once the patient is in remission, the drug should be reduced or discontinued immediately.
Intravenous lidocaine is an option when acute myocardial infarction is complicated by ventricular prematureness, and intravenous procainamide can be administered in cases where lidocaine is ineffective. Although these drugs to suppress ventricular prematureness have not reduced in-hospital mortality in patients in clinical use.
Careful selection of radiofrequency ablation for ventricular prematureness
Many patients believe that excessive ventricular prematureness affects cardiac function and general health and are eager to be cured by radiofrequency ablation. Radiofrequency ablation can indeed cure ventricular prematureness, but it is worth emphasizing that radiofrequency ablation for ventricular prematureness is still a Class IIb indication, which means that this treatment should not be used if possible. In addition, when patients are considering radiofrequency ablation treatment, they should also choose a well-equipped hospital and an experienced physician to receive the treatment selectively.
The indications for radiofrequency ablation of ventricular premature include excessive total number of ventricular premature (>10,000/day), high level of associated symptoms, existing or potential cardiac insufficiency, and low natural variability of ventricular premature. Therefore, the majority of ventricular premature is not easy or suitable for radiofrequency ablation treatment, coupled with the high cost of the procedure, certain failure rate and recurrence rate, so the choice must be extra important.