Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperventilation is well known to affect the electrocardiogram (ECG) in subjects without heart disease and produce spasm in patients with variant angina. The autonomic nervous system is thought to play a significant role in these effects. However, the normal hemodynamic response to hyperventilation is not well defined. We subjected 369 healthy volunteers (200 men, 169 women) to prolonged hyperventilation (30 respirations for 5 min and 10 min recovery) under continuous ECG monitoring and to exercise testing. Heart rate (HR), systolic and diastolic blood pressures (SBP, DBP) and rate-pressure product were recorded. Hyperventilation resulted in an immediate (within the first min), significant increase in HR by 27.4%, a further small increase at min 2 of hyperventilation, and a subsequent small decrease in HR at mins 3-5. An immediate drop of HR by 20.1% was observed with discontinuation of hyperventilation. Apart from a slightly higher HR increase in men, a similar pattern of HR changes was found in both genders. On multivariate analysis, younger age, absence of smoking, and male gender were associated with a higher HR increase with hyperventilation (p < 0.0001, p < 0.0001, and p < 0.001, respectively). SBP and DBP increased with hyperventilation, with their highest value at min 5 of hyperventilation and a subsequent drop to baseline levels. Age and gender did not affect the degree and pattern of BP changes. Absence of smoking and the presence of hypertension were associated with a higher SBP with hyperventilation (p < 0.003 and p < 0.007). The rate-pressure product increased by 43.6% with hyperventilation, a change that was only 19.1% of the respective rate-pressure product observed with exercise. Hyperventilation results in significant HR and BP increases, changes that are influenced by age, gender, smoking, and hypertension. Our study could serve as a standard for comparison of the hyperventilation effects in different disease states.
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PMID:Hemodynamic response to hyperventilation test in healthy volunteers. 859 May 32

This study was designed to examine the ventricular vulnerability of patients with vasospastic angina. Fourteen patients (mean age 57 +/- 9 years) with vasospastic angina underwent electrophysiologic testing during the asymptomatic phase (baseline) and after the relief of acetylcholine-induced spasm with isosorbide dinitrates. Twenty patients without structural heart disease served as a control group. By programmed ventricular stimulation, polymorphic ventricular tachycardia (VT) was induced at baseline in 6 of 14 patients, with 1 patient developing ventricular fibrillation and 7 of 14 patients developing repetitive ventricular responses. After isosorbide dinitrate, polymorphic VT was induced in only 1 patient who had ventricular fibrillation at baseline. Repetitive ventricular responses were induced in 3 of 5 patients who had VT at baseline and in 4 of the 7 patients with repetitive ventricular responses at baseline. There was a significant difference in the incidences and severity of induced ventricular arrhythmias between the 2 phases (p <0.01). Among 20 control subjects, repetitive ventricular responses were induced only in 6 patients, but no VT was induced. There was a significant difference in the incidence of induced ventricular arrhythmias and VT at baseline between the vasospastic angina and control groups (p <0.001 and <0.01, respectively). Thus, patients with vasospastic angina had increased ventricular vulnerability, even during the symptom-free period without ischemic events, which could predispose to the development of life-threatening arrhythmias aggravated by vasospastic attacks.
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PMID:Induction of polymorphic ventricular tachycardia by programmed ventricular stimulation in vasospastic angina pectoris. 860 62

Patients with systemic sclerosis (SS) have cardiac dysfunction induced by cold exposure. We and others have demonstrated this finding after corporal chilling, suggesting a "coronary Raynaud phenomenon" mediated by intermittent vascular spasm. In this study we evaluated the effect of diltiazem (DTZ) in cardiac dysfunction induced by cold test in patients with SS without clinical evidence of heart disease. Twelve patients with SS were studied. One patient was excluded because he did not fulfill the prescribed treatment. Eleven patients (age of 49.9 +/- 3.8 years and illness duration of 9.3 +/- 4.8 years) were included. Gated equilibrium radionuclide ventriculography was recorded after red blood cells were labeled in vivo using an intravenous injection of stannous pirophosphate followed by 20 mc of 99 Tc (gamma camera with electrocardiographic R wave gating was used). Left ventricular injection fraction (LVEF) was calculated using computer analysis and wall motion abnormalities by visual interpretation. Patients were cooled using a thermic blanket set at 5 degrees centigrade. They were evaluated before and after a period of cooling. After corporal chilling LVEF decreased more than 10% in all of them. DTZ 270 mg a day was administered to the same patients during 48 hs. Basal and cold LVEF were repeated in all patients. The results with and without DTZ were compared by Student's t Test. The basal LVEF with and without DTZ was not different (64.8 +/- 2.6 and 63.1 +/- 1.8). After corporal chilling LVEF decreased (64.8 +/- 2.6 to 54.8 +/- 2.5 p < 0.00001) and reversible abnormalities in wall motion were noticed in patients without DTZ. When they received DTZ neither difference in LVEF (63.1 +/- 1.8 to 62.1 +/- 2.4) nor wall motion abnormalities were observed. We compared the LVEF after chilling (62.1 +/- 2.4 and 54.8 +/- 2.5) and we found an important difference with the use of DTZ (p < 0.005). It can be concluded that in patients with SS and no overt heart disease, DTZ prevents the early cardiac dysfunction induced by cold test. Probably this drug blunts the coronary spasm induced by cold test in this group of patients.
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PMID:[Effect of diltiazem on cold-induced left ventricular dysfunction in patients with systemic sclerosis]. 943 69

We report the cases of three young men, heavy smokers, without previous heart disease and who were resuscitated after cardiac arrest due to ventricular fibrillation attributed to coronary spasm. All of them complained of atypical chest pain and the exercise testing, echocardiogram and coronary angiography were normal. The first case was diagnosed by Holter monitoring and by provocative testing with intracoronary ergonovine; the second by provocative testing with intracoronary acetylcholine and the third by Holter monitoring. The patients were treated with a calcium antagonist and/or nitrates and in the follow up they remained asymptomatic.
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PMID:[Coronary spasm and heart arrest caused by ventricular fibrillation]. 964 68

Magnesium has been reported to have a dilatatory effect on cerebral arteries. Reduction of extracellular Mg+2 has been shown to be directly correlated with the intensity of cerebral spasm. A neuroprotective effect of magnesium in stroke has also been hypothesized. The aim of our study was to examine the Mg+2 levels in serum and cerebrospinal fluid (CSF) in the early stage of stroke and to evaluate the correlation between Mg+2 levels and the development of neurological deficits. Between 1986 and 1994, 96 patients who had a stroke of 24- to 48-h duration were enrolled in the study. Serum and CSF levels of magnesium were checked on admission, 2448 h after the onset of stroke. Using a neurological score, the neurological deficit was assessed on the 1st day, 1 and 4 weeks later. Computed tomography (CT) was performed after 1 week, and the volume and location of infarction were calculated and measured. Statistical analysis was performed for cortical and subcortical patients separately, using Spearman correlation and multiple linear and logistic regression analyses. Significant correlation was found between CSF Mg+2 and the size of the infarct (P < 0.0001). There was no correlation between serum Mg+2 and CSF Mg+2 levels. Regression analysis demonstrated an increase in the values of the Mathew Neurological Score with higher CSF Mg+2 levels. This association remained true after other factors such as age, associated heart disease, diabetes and infarction size had been taken into account by the regression model. The results confirm that there is a relationship between a low Mg+2 concentration in CSF during the first 48 h after onset of ischaemic stroke and the intensity of the neurological deficit. The therapeutic consequence of this finding may have some importance.
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PMID:Cerebrospinal fluid magnesium level as a prognostic factor in ischaemic stroke. 975 95

This study examines the incidence of spasm by intracoronary injection of acetylcholine in Japanese patients who underwent coronary angiography. The subjects were 685 consecutive patients (477 men, mean age 63.2 +/- 7.5 years) who were studied with an acetylcholine test. Acetylcholine was injected in incremental doses of 20, 50, and 80 microg into the right coronary artery and 20, 50, and 100 microg into the left coronary artery. Spasm was defined as total or subtotal occlusion. Coronary vasospasm was determined in 221 patients (32.3%). Spasm occurred often during effort and rest in patients with angina (25 of 51, 49.0%), exertional angina (25 of 74, 33.8%), recent myocardial infarction (30 of 80, 37.5%), healed myocardial infarction (14 of 37, 37.8%), and especially in patients with rest angina (83 of 124, 66.9%), whereas spasm was relatively uncommon in patients with nonischemic heart disease (23 of 252, 9.1%). Spasm was superimposed on significant atherosclerotic lesions in 35.9% of patients as well as on nonfixed atherosclerotic lesions in 30.8% of patients. We conclude that >9% of Japanese patients may have coronary vasospasm with intracoronary injection of acetylcholine and recommend the provocation test for evaluating coronary vasospasm if coronary angiography is undertaken.
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PMID:Frequency of provoked coronary vasospasm in patients undergoing coronary arteriography with spasm provocation test of acetylcholine. 1021 81

Chagas' disease, caused by the parasite Trypanosoma cruzi, is an important cause of heart disease. Previous studies from this laboratory revealed that microvascular spasm and myocardial ischemia were observed in infected mice. Infection of endothelial cells with this parasite increased the synthesis of biologically active endothelin-1 (ET-1). Therefore. in the myocardium of T. cruzi-infected mice, we examined ET-1 expression and the p42/44-mitogen activated protein kinase (MAPK)-AP-1 pathway that regulates the expression of ET-1. There was parasitism and myonecrosis in the myocardium of infected C57BL/6 mice. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed elevated mRNA expression of transcription factor AP-1 (c-jun and c-fos) and increased AP-1 DNA binding activity as determined by electrophoretic mobility shift assay (EMSA). Western blot analysis demonstrated an increase in the phosphorylated forms of extracellular signal-regulated kinase (ERK1/2). ET-1 mRNA was upregulated in the myocardium of infected mice. Immunohistochemical and immunoelectron microscopy using anti-ET-1 antibody detected increased expression in cardiac myocytes and endothelium of these mice. These data suggest that ET-1 contributes to chagasic cardiomyopathy and that the mechanism of the increased expression of ET-1 is a result of the activation of the MAPK pathway by T. cruzi infection.
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PMID:Trypanosoma cruzi infection (Chagas' disease) of mice causes activation of the mitogen-activated protein kinase cascade and expression of endothelin-1 in the myocardium. 1107 62

Chagas' disease, caused by the protozoan parasite Trypanosoma cruzi, is an important cause of cardiomyopathy. Microvascular spasm and matrix dissolution, modulated by endothelin-1 (ET-1), is implicated in the pathogenesis of chagasic heart disease. To further elucidate the role of ET-1 in murine chagasic heart disease, C57BL/6 x 129sv mice were infected with T. cruzi (10(3) trypomastigotes of the Brazil strain). These mice are resistant to death during the acute phase but progress to chronic cardiomyopathy. Infected mice were compared with infected mice treated with phosphoramidon, a non-specific metalloprotease inhibitor that is also a potent inhibitor of endothelin-converting enzyme, at a dose of 10 mg/kg. Mice were treated with phosphoramidon for the initial 15 days post infection (PI). All mice were evaluated 200 days PI. Examination of infected, untreated mice revealed marked inflammation, vasculitis and fibrosis. The hearts of infected treated mice had significantly less pathology. Cardiac magnetic resonance imaging (MRI) revealed that right ventricular internal diameter (RVID) was significantly greater (P<0.05) in the infected untreated group (2.9+/-0.22 mm) as compared with the infected treated group (1.73+/-0.35 mm). In another experiment phosphoramidon treatment was also tested in CD1 mice, which have a high mortality during the acute phase of infection with 5 x 10(4) trypomastigotes of the Brazil strain. One group of CD1 mice was untreated while the other group received phosphoramidon for the initial 15 days PI. The mortality rate in untreated mice was 70% by day 35 PI, while all treated infected mice lived. The parasitemia in both groups was similar. The cardiac pathology was more severe in untreated mice. MRI revealed the RVID to be significantly greater in the untreated infected group as compared with the phosphoramidon-treated infected mice (2.74+/-0.03 mm versus 1.64+/-0.4 mm P<0.05). Transthoracic echocardiography revealed that the percentage fractional shortening was reduced in infected CD1 mice but not in those infected mice treated with phosphoramidon. There was no effect of phosphoramidon in uninfected mice. Phosphoramidon (100 microg/ml) had no effect on parasites in vitro. These data are consistent with the hypothesis that ET-1 contributes to the pathogenesis of murine chagasic cardiomyopathy and suggests that interventions targeting ET-1 would improve the outcome in chagasic heart disease.
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PMID:Phosphoramidon treatment improves the consequences of chagasic heart disease in mice. 1219 1

A 67-year-old female with recurrent syncope and no obvious heart disease developed ventricular dysfunction, known as takotsubo cardiomyopathy, following a 90 s episode of polymorphic ventricular tachycardia originating from a ventricular extrasystole with a short coupling interval. Cardiac catheterization performed 30 min after the arrhythmic event revealed angiographically normal coronary arteries, and left ventricular apical akinesis and basal hyperkinesis. An intracoronary injection of acetylcholine revealed no inducible coronary spasm, and an electrophysiological study revealed normal atrioventricular conduction and no inducible ventricular arrhythmia. Thirty hours after the arrhythmic event, electrocardiography revealed deeply inverted T waves in leads V3 to V6, I, and aVL, which continued for more than a week. Although no treatment was given to maintain hemodynamic stability, echocardiography revealed normal left ventricular contraction 14 days after the onset of the ventricular dysfunction. The reversible ventricular dysfunction might have been induced by altered catecholamine dynamics due to the persistent syncope during the occurrence of tachycardia.
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PMID:Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia. 1270 94

We thoroughly examined a 26-year-old Japanese male who experienced perioperative ventricular tachycardia. After inhaling sevoflurane, his nasal cavity was soaked with 1:100,000 epinephrine and he was intubated through the nose. Junctional tachycardia occurred five minutes after intubation, changing to ventricular tachycardia. Six-time cardioversion was required to stop the ventricular tachycardia. Echocardiography immediately following the event showed diffuse hypokinesis, and an electrocardiogram showed an inversion of T waves in II, III, aVF and V4-6. Both returned to normal within a few days. Tl scintigraphy revealed a normal perfusion image. Coronary angiography showed a normal coronary, but an injection of acetylcholine induced vasospasm in the right coronary artery. Examination of left ventricular tissue yielded no specific findings. During electrophysiological tests, ventricular tachycardia could not be induced even in the presence of isoprenaline. This is a very young case to elicit vasospasm in the coronary artery with no underlying heart disease. Although the relationship between perioperative ventricular tachycardia and coronary spasm is unknown, cardiac events can occur during anesthesia in young and low-risk patients.
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PMID:Coronary artery spasm discovered in thorough examination of perioperative VT in a 26-year-old Japanese male. 1471 Nov 96


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