Analysis of the antihypertensive effect of nifedipine Clinical efficacy. Object and Methods 1.1 Object: Hospital inpatients, 42 cases, including 25 male cases, 17 female cases, aged between 35 to 75 years, with an average age of 52 years. The primary diseases were ischemic cardiomyopathy, dilated cardiomyopathy, and rheumatic heart disease. Classification was done according to the NYHA Standard for cardiac function, with seven cases of cardiac function II, 21 cases of cardiac function III, and 14 cases of cardiac function IV. Measurements were taken after admission, including serum potassium and magnesium concentration, determination of 24h ambulatory ECG, echocardiography, and cardiac function. After oral administration of spironolactone at 120mg/day, Monopril (fosinopril) at 10 to 20mg/day, in conjunction with the use of digitalis and diuretics, dobutamine, medication was reviewed after six weeks for serum ion, 24-hour ambulatory ECG, echocardiography, and cardiac function determination. 1.2 Observation Standards: CX100 automatic biochemical analyzer determined serum ion changes before and after treatment, the value of 24h PI company Hoher monitoring system compared ventricular arrhythmias occurrence before and after treatment. Acuson128XP/10 color Doppler audio-visual instrument compared left ventricular end-diastolic diameter and left ventricular ejection fraction (EF). I. 3 Statistical Analysis: Measurement data are expressed as mean ± standard deviation (i ± s), comparisons before and after treatment used the t-test, P < 0.05, significant meaning. 2 Results 2.1 Serum Ion Changes: Serum potassium stabilized within the normal range, no hyperkalemia or hyperlipidemia. Magnesium levels were below normal or low before treatment but significantly increased after treatment. 2.2 24h Ventricular Arrhythmia Monitoring: Ventricular arrhythmias decreased after treatment, and some patients with short ventricular tachycardia disappeared after treatment. Observed indicators of change 2.3 Table 1 Before and After Treatment, Echocardiography, and Cardiac Energy Change: Left ventricular end-diastolic diameter (LVDD) significantly narrowed. EF before treatment was less than 45% and increased after treatment. Shown in Table 1. 3 CHF is a complex circulatory congestion, left ventricular systolic function damage, and neuroendocrine system activation clinical syndrome. (Myocardial infarction, hemodynamic overload, inflammation), causing changes in myocardial structure and function, which is a kind of disease due to any reason, initially myocardial injury. The basic mechanisms that lead to the development of heart failure are ventricular remodeling. Ventricular remodeling is a complex series of molecular and cellular mechanisms leading to changes in cardiac structure, function, and phenotype. After the initial myocardial injury, various endogenous neuroendocrine and cytokine activations promote left ventricular remodeling. Heart failure occurs when the heart's cardiac output cannot meet the body's needs, resulting in the activation of the sympathetic nervous system. The renin-angiotensin-aldosterone system (RAAS), thus increasing neurohormonal compensatory increase. Two metabolites in the renin-activated angiotensin II and aldosterone increase the degree of CHF severity positively correlated. They can cause sodium and water retention, serum potassium and magnesium loss, peripheral vasoconstriction, worsening heart failure. RAS organizes endocrine (autocrine and paracrine) and circulating endocrine work; the role of endocrine organization is particularly important in chronic heart failure. In heart failure, myocardial angiotensin-converting enzyme (ACE) activity increases; angiotensinogen (mRNA) levels rise; density of angiotensin II receptor (AT), the RAS plays a key role in myocardial remodeling. This allows ACEI angiotensin-I not to be converted into angiotensin II (A II), reducing A II production, thereby inhibiting the adverse effects of A II. On the other hand, ACE and slow shock peptidase II are the same, therefore, ACEI degradation of bradykinin reduces strengthening bradykinin; promoting prostacyclin 1_ nitric oxide synthesis. The kinin strengthening role is equally important. Increase in aldosterone release can improve cardiac function in a short period of time, playing a compensatory role in cardiac function, but long-term increase in aldosterone levels causes sodium retention, electrolyte imbalance, myocardial fibrosis, increased cardiac arrhythmia. ACEI may confront the role of RAAS 3 to 12 months after treatment. ACE concentration is normal or low aldosterone levels began to rise ACEI cannot sustainably inhibit aldosterone, direct aldosterone antagonist spironolactone treatment of CHF. Based on the above theory, combining monopril and spironolactone for treating CHF, observing the effect from changes in the occurrence of ventricular arrhythmias, serum potassium and magnesium ions change, LVDD, and EF. As a result, ventricular arrhythmias significantly decreased, serum magnesium ions elevated, without causing hyperkalemia, reduce LVDD, EF increases, receiving a good clinical effect.