Progress in cardiovascular diseases
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Prog Cardiovasc Dis · Sep 1995
ReviewRole of nitric oxide in the regulation of myocardial function.
Nitric oxide (NO), produced by either constitutive or inducible isoforms of NO synthase (cNOS or iNOS), influences myocardial inotropic and chronotropic responses. This pathway has been studied using NO donors or NOS inhibitors or by immune-mediated stimulation of iNOS. Although inhibition of constitutive NO activity in the heart does not influence indices of myocardial contractility, NO donors, in some species and preparations, may exert a negative inotropic effect as well as an enhancement of diastolic relaxation. ⋯ NO-stimulated production of 3',5'-cyclic guanosine monophosphate via guanylyl cyclase accounts for many of the observed physiological actions of NO. 3',5'-Cyclic guanosine monophosphate inhibits the beta-adrenergic-stimulated increase in the slow-inward calcium current and reduces the calcium affinity of the contractile apparatus, actions that could contribute to a negative inotropic effect, an abbreviation of contraction, and an enhancement of diastolic relaxation. Biochemical, immunocytochemical, and molecular biological techniques have been used to show the presence of both cNOS and iNOS within the myocardium. cNOS is expressed in myocytes, endothelial cells, and neurons in the myocardium, and there is evidence for iNOS in myocytes, small vessel endothelium, vascular smooth muscle cells, and immune cells that infiltrate the heart. Taken together, these observations suggest that NO influences normal cardiac physiology and may play an important role in the pathophysiology of certain disease states associated with cardiac dysfunction.
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Prog Cardiovasc Dis · Jan 1993
ReviewVariation in late potentials and the reproducibility of their measurement.
The usefulness of a test depends on its reproducibility. This determines how closely the test result indicates the actual pathophysiologic state, how well it will predict that state in the future, and if interventions or further pathologic changes are reflected by the test. There is a variation in the parameters of the signal-averaged ECG, more so with spectral than with time domain measurements. ⋯ And perhaps the relationship must be tested independently for each drug assessed. In the same regard, there is much excitement about the benefits of thrombolytic therapy, but when diagnosing benefit to the individual patient we have to remember the lack of reproducibility of the measurements and also keep in mind that an improved signal-averaged ECG cannot be translated into an improved prognosis without long-term controlled studies. In summarizing the variation and reproducibility of measurements made from the signal-averaged ECG we avoided providing more than a sense of the extent of variation expected because precise confidence intervals depend on the particular techniques used to make the measurements.(ABSTRACT TRUNCATED AT 400 WORDS)
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Prog Cardiovasc Dis · May 1985
ReviewCardiovascular manifestations of systemic lupus erythematosus: current perspective.
Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. ⋯ It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)