Modern medicine has been used to treat myocardial infarction, a subset of cardiovascular diseases, and have been relatively effective but not without adverse effects. Consequently, this issue has stimulated interest in the use of natural products, which may be equally effective and better tolerated. Many studies have investigated the cardioprotective effect of natural products, such as plant-derived phytochemicals, against isoproterenol (ISO)-induced myocardial damage; these have produced promising results on the basis of their antioxidant, anti-atherosclerotic, anti-apoptotic and anti-inflammatory activities. This review briefly introduces the pathophysiology of myocardial infarction (MI) and then addresses the progress of natural product research towards its treatment. We highlight the promising applications and mechanisms of action of plant extracts, phytochemicals and polyherbal formulations towards the treatment of ISO-induced myocardial damage. Most of the products displayed elevated antioxidant levels with decreased oxidative stress and lipid peroxidation, along with restoration of ionic balance and lowered expression of myocardial injury markers, pro-inflammatory cytokines, and apoptotic parameters. Likewise, lipid profiles were positively altered and histopathological improvements could be seen from, for example, the better membrane integrity, decreased necrosis, edema, infarct size, and leukocyte infiltration. This review highlights promising results towards the amelioration of ISO-induced myocardial damage, which suggest the direction for future research on natural products that could be used to treat MI.

Vasovagal syncope (VVS) is the commonest cause of syncope accounting for up to 60% of all cases. The head-up tilt-table test (HUTT) was first described as a diagnostic test for VVS in 1986 and is now in widespread use as a research and diagnostic tool. Vasovagal syncope was previously thought to be confined to younger patients but with the introduction of HUTT, it is now being diagnosed with greater frequency in the elderly. Research into the physiological changes in susceptible individuals during HUTT has greatly increased our understanding of the pathophysiological processes underlying VVS; in particular, the hypotensive response during VVS is associated with sympathetic withdrawal rather than bradycardia alone. Various provocation agents, including nitrates, isoprotenerol and lower body negative pressure have been described to improve the diagnostic yield of the HUTT. Glyceryl trinitrate is now routinely administered during HUTTs. Individuals with typical presentations and infrequent episodes do not require investigation with HUTT as history alone is often diagnostic. The head-up tilt-table test is, however, required with atypical features, seizure activity, occupational issues, and is more likely to be required in older patients. The practicalities of conducting the HUTT and limitations of HUTTs are also discussed.

A 20-year-old white judoka was admitted for severe palpitations during exercise followed by syncope. The electrocardiogram on admission revealed a wide-complex monomorphic tachycardia at a rate of 260 beats/min, with right bundle brunch block morphology and right axis deviation. Following electrical cardioversion, the electrocardiogram showed sinus rhythm with type 1 pattern of Brugada syndrome. We describe in detail the clinical course, the results of electrophysiological study, and therapeutic management. We reviewed literature data concerning a few cases of \'atypical Brugada syndrome\' characterized by monomorphic ventricular tachycardia as clinical arrhythmia.

Carditis is a common manifestation of adult patients with Lyme disease affecting 4-10% of Lyme patients in the United States. However, children with Lyme disease rarely present with acute carditis. The management of pediatric patients with complete heart block (CHB) secondary to Lyme carditis has not been well described. We report the acute management of 2 pediatric patients that presented in CHB secondary to Lyme disease.

暂无摘要。

暂无摘要。

暂无摘要。

暂无摘要。

1. There has been considerable debate whether responses mediated via beta1- and beta2-adrenoceptors (beta1ARs and beta2ARs) display the same degree of desensitization after prolonged or repeated exposure to agonists. 2. Examples are provided for selective desensitization of functional responses and loss of binding sites for beta1ARs. Equally, examples are given of selective desensitization and down-regulation involving beta2ARs. 3. This review examines whether receptor subtype-selective desensitization of betaAR-mediated responses can occur and whether even within the same subtype, there may be tissue-selective desensitization. Possible reasons why apparent selectivity of desensitization of functional responses may occur are considered and are divided into methodological and non-methodological factors. 4. Methodological factors discussed are: the concentration of agonist used for inducing desensitization and the washout times before construction of the post-incubation concentration-response curve (CRC), the need for correction of CRCs from time-matched controls, and the methods adopted for plotting CRCs. 5. Four non-methodological factors are considered. Firstly, the roles of different receptor reserves for the responses of each tissue can have an important effect on whether desensitization is apparent; a large reserve will make desensitization less likely to be apparent. Secondly, there is more than one site at which desensitization occurs; receptors are uncoupled from adenylyl cyclase activation, there is an additional site at the level of stimulation of cyclic AMP-dependent protein kinase and betaARs may ultimately be down-regulated. These processes may differ depending on the tissue and conditions and this may influence whether differential desensitization occurs between tissues. Thirdly, the apparent degree of desensitization after washout of an agonist can depend upon the rate of resensitization. Experiments to overcome this problem are described which demonstrate betaAR desensitization in the continued presence of agonist. Finally, the role of up-regulation of PDE in desensitization is discussed.

BACKGROUND: Upright tilt testing is widely utilized for the evaluation of syncope. Recently, there have been concerns about the specificity and the lack of standard methodology for this test. The purpose of this study was to summarize the methodologies of upright tilt testing in patients with syncope of unknown origin, the responses in control subjects, and the reproducibility and selection of therapy.
METHODS: We used MEDLINE to search English language articles from 1966 to June 30, 1992. Studies were included for content review if they met our inclusion criteria. Data were extracted from each article by two trained reviewers using a predesigned data collection instrument.
RESULTS: Thirty-three articles were included for review. There was considerable variability in the methodologies of tilt testing. Overall positive responses were reported in 49% of patients in passive-only studies as compared with 66% of patients in studies using isoproterenol with tilt testing. The percentage of positive responses increased with increasing angle of testing for studies using isoproterenol. There was no relationship between the percentage of positive responses and the maximum dose of isoproterenol. When we compared the results of passive studies that tested patients for 60 minutes at 60 degrees with the results of isoproterenol studies that tested patients at 60 degrees, the positive rate for passive-only studies was 54% as compared with 52% for the isoproterenol studies. The percentage of positive response in control subjects with passive studies was 8.9% (range 0% to 100%), and with isoproterenol 27% (range 0% to 65%). Other groups of patients showed a wide range of positive responses (range 0% to 83%). Reproducibility ranged from 71% to 87%. Upon retesting while the patient was receiving therapy, 90% of 115 positive patients were negative. Eighty-nine percent of 105 positive patients who were receiving therapy and followed for a mean time of 12 months were free of syncope.
CONCLUSIONS: This review strongly suggests that isoproterenol may not have an effect on stimulating vasovagal syncope during upright tilt testing. We recommend protocols of passive tilt testing procedures at 60 degrees for 45 to 60 minutes since the overall specificity is higher with this method. The use of isoproterenol during tilt testing adds to the cost and complexity of the test, is associated with a higher rate of false-positive responses, leads to potential complications, and, thus, should be avoided.