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by yt444827528 on 2012-03-05 14:34:10

**Analysis of 15 Cases of Conduction Dysfunction Complicated by Myocarditis in Typhoid Fever**

Fifteen cases of conduction dysfunction complicated by myocarditis due to typhoid fever were analyzed. Blood cultures were positive in 12 cases, with titers ranging from 1:320 to 1:1280. All child cases were positive. Electrolytes were within normal limits in 15 cases. Upon admission, all cases underwent ECG examination, which showed normal or nearly normal results. Between 7 and 10 days, patients experienced chest tightness, palpitations, dizziness, and fatigue but did not blindly take medication. Auscultation revealed arrhythmia in nine cases.

Electrocardiogram (ECG) findings: sinoatrial block and/or widened sinus stroke in five cases, first-degree atrioventricular block in two cases, second-degree type I atrioventricular block in four cases, second-degree type II atrioventricular block in one case, complete right bundle branch block in one case, and left bundle branch block in one case. Repeated electrolyte tests were normal, and echocardiography was also normal.

Treatment and Outcome: Initially, treatment was challenging for all cases, as they presented with unexplained fever lasting 5-7 days, with the intention of monitoring until the fever subsided. Once confirmed, the diagnosis was made, and anti-typhoid treatment with ampicillin + ofloxacin, ampicillin + tetracycline, or tetracycline + ofloxacin was administered. Simultaneously, supportive care and enhanced myocardial protection were provided. If necessary, hormones were used. Symptoms disappeared after 10-15 days. Follow-up ECGs showed that one case exhibited second-degree type II atrioventricular block, while the remaining 14 cases were normal. Other typhoid-related symptoms, such as fever and liver dysfunction, also returned to normal. One case of second-degree type II atrioventricular conduction block showed normal ECG results six months after follow-up.

Discussion: Typhoid fever may be complicated by various complications. The incidence of toxic myocarditis follows intestinal bleeding and typhoid hepatitis. In this group of cases, a clear diagnosis of typhoid fever was made 2-3 weeks into the illness based on clinical symptoms and ECG findings, followed by appropriate treatment. All cases of typhoid fever and myocarditis resolved clinically, confirming the diagnosis of typhoid fever complicated by myocarditis.

Clinical features of typhoid fever complicated by viral myocarditis include: rapid heart rate, reduced first heart sound, cardiac arrhythmias, systolic and diastolic gallop rhythm, and blood pressure changes. ECG findings show prolonged P-R intervals and ST-T abnormalities. Reports of cardiac conduction dysfunction are rare. Cardiac conduction dysfunction is commonly seen in myocarditis, coronary heart disease, myocardial infarction, cardiomyopathy, cardiac surgery, trauma, congenital deformities, unexplained fibrosis affecting the pumping system, hyperkalemia, certain drug toxicities (e.g., digitalis), hypoxia, vagus nerve stimulation, and hyperthyroidism.

The pathogenesis of toxic myocarditis complicating typhoid fever involves three aspects: (1) direct effect of *Salmonella typhi* on the myocardium; (2) damage to myocardial cells caused by the release of endotoxins from *Salmonella typhi*; (3) during treatment, large numbers of typhoid bacilli killed by strong bactericides act as allergens, releasing large amounts of dead bacteria and endotoxin decomposition products, triggering hypersensitivity reactions in body tissues, leading to myocardial injury. The severity of myocardial injury depends on bacterial virulence and toxin quantity.

Myocarditis may involve diffuse or localized lesions of the myocardium, potentially affecting the cardiac pacemaker and conduction system, such as the atrioventricular node, atrioventricular bundle, and bundle branches. Clinical manifestations depend on the extent and location of the lesion, ranging from sudden death to asymptomatic cases. In this group of cases, the role of *Salmonella typhi* or its toxins/decomposition products in the cardiac conduction system likely caused localized myocardial damage and conduction dysfunction.

Therefore, when treating typhoid fever patients, potential cardiac damage should be vigilantly monitored. If relevant symptoms occur, ECG should be promptly performed. Concurrent treatment of related lesions should include active and appropriate measures to avoid further cardiac function impairment.