BackgroundCardiac shock wave therapy (CSWT) improves cardiac function in patients with severe coronary artery disease (CAD). We aimed to evaluate the clinical outcomes of a new CSWT treatment regimen.MethodsThe 55 patients with severe CAD were randomly divided into 3 treatment groups. The control group (n = 14) received only medical therapy. In group A ( n = 20), CSWT was performed 3 times within 3 months. In group B ( n = 21), patients underwent 3 CSWT sessions/week, and 9 treatment sessions were completed within 1 month. Primary outcome measurement was 6-minute walk test (6MWT). Other measurements were also evaluated.ResultsThe 6MWT, CCS grading of angina, dosage of nitroglycerin, NYHA classification, and SAQ scores were improved in group A and B compared to control group.ConclusionsA CSWT protocol with 1 month treatment duration showed similar therapeutic efficacy compared to a protocol of 3 months duration.Clinical trial registryWe have registered on ClinicalTrials.gov, the protocol ID is CSWT IN CHINA.

Background: Safe and effective therapeutic management of refractory coronary artery disease (CAD) in heart patients is critical to enhance cardiovascular function and improve quality of life. Current therapies for refractory CAD are inadequate in ameliorating angina and promoting revascularization of ischemic myocardium. Hypothesis: Cardiac shock wave therapy (CSWT) is a safe and effective noninvasive intervention in the management of patients with refractory CAD. Methods: The study enrolled 9 male patients age 50 to 70 years (5.11 ± 5.46 years) with a diagnosis of CAD and stent implantation (3.00 ± 2.24 stents). CSWT was carried out for 3 months at 3 intervals during the first week of each month (first, third, and fifth day), for a total of 9 therapies per patient. Dobutamine stress echocardiography and radionuclide angiography identified the myocardial ischemic segments. The effects of CSWT on myocardial perfusion and systolic function were examined. Other outcome measures included myocardial injury enzyme markers, angina scale, nitroglycerin dosage, and cardiopulmonary fitness assessments. Results: Improved myocardial blood flow and regional systolic function (stress peak systolic strain rate −1.10 to −1.60 s −1 , P = 0.002) were detected in patients following CSWT. Reductions in creatine kinase (87.89 ± 36.69 to 86.22 ± 35.96 IU/L, P = 0.046), creatine kinase MB (10.89 ± 5.73 to 10.11 ± 5.93 IU/L, P = 0.008), aspartate transaminase (interquartile range [IQR], 28.00 to 27.00 IU/L, P = 0.034) were also found. Angina (Canadian Cardiovascular Society scale IQR 3.0 to 2.0, P = 0.035) and nitroglycerin dose reduction (IQR 3.0 to 1.0 times/wk, P = 0.038) were reported.Conclusions: This study is a preliminary assessment of CSWT in patients with refractory CAD. We report that CSWT is a noninvasive, effective, and safe intervention in the treatment of refractory CAD.

The results show that SW therapy ameliorates myocardial fibrosis after AMI in pigs, which is associated with the decreased amount of fibrocytes.

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The aim of this study was to investigated the functional changes of airway epithelial cells and mitochondria in rat models of asthenic lung and phlegm blocking combined with cough variant asthma (CVA). Sixteen Sprague-Dawley rats were randomly divided into two groups: Control and model group, with 8 rats in each group. On the basis of the CVA rat model induced and sensitized by ovalbumin and aluminum hydroxide, the rat models with asthenic lung and phlegm blocking combined with CVA were established via smoking stimulation. The rats in the control group were injected with equivalent normal saline. All rats were sacrificed after the model was successfully prepared. The lung histopathological sections of the two groups of rats were observed, and respiratory control ratio (RCR) of mitochondria and membrane potential changes were compared. The results showed that the rats in the model group had tracheal structure abnormities, epithelial cell damages, cilia structure defects, capillary injection, alveolar exudates, and inflammatory cells compared to those in the control group. RCR of mitochondria and membrane potential of rats in the model group were significantly lower than those of rats in the control group (P<0.05). Damaged lung tissue and decreased mitochondrial activity and membrane potential are detected in the rat models of asthenic lung and phlegm blocking combined with CVA.