Showing papers in "European Heart Journal in 1993"

An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man

Abstract: Amplification of the pressure pulse between central and peripheral arteries renders pressure values in the upper limb an inaccurate measure of ascending aortic (AA) pressure. Accuracy could be improved by allowance for such amplification. Transfer functions (TF) for pressures between AA and brachial artery (BA): (BATF) and between AA and radial artery (RA): (RATF) were derived from high-fidelity pressure recordings obtained at cardiac catheterization in 14 patients under control conditions, and after sublingual nitroglycerine 0.3 mg. There was no significant difference in BATF under control conditions and with nitroglycerine; hence results were pooled. Control and nitroglycerine results were also pooled to obtain a single RATF. BATF and RATF moduli peaked at 5 Hz and 4 Hz, reaching 2.5 and 2.8 times the value at zero frequency respectively. Frequency-dependent changes in modulus and phase of BATF and RATF were attributable to wave travel and reflection in the upper limb. BATF and RATF were compared to published transfer functions and those derived from analysis of aortic and brachial or radial pressure waves in previous publications. Results were similar. Our BATF and RATF were used to synthesize AA pressure waves from published peripheral pulses. Correspondence was close, especially for systolic pressure which d by 2.4 ± 1.0 (mean ± SEM) mmHg, whereas recorded systolic pressure differed by 20.4 ± 2.6 (mean ± SEM) mmHg between central and peripheral sites. Results indicate that in adult humans a single generalized TF can be used with acceptable accuracy to determine central from peripheral pressure under different conditions. While this process is capable of refinement, it represents an advance on the present practice of assuming that central and peripheral pressures are identical.

The multicenter-european-radiofrequency-survey (merfs) - complications of radiofrequency catheter ablation of arrhythmias

Abstract: Radiofrequency (RF) catheter ablation has developed into a new non-pharmacological therapy for the definitive treatment of patients with cardiac arrhythmias. Although an increasing number of recent reports have indicated the widespread use of the procedure, no data are available to estimate the number of procedures performed in Europe. Furthermore, currently no data on a large series of patients are available that provide information on the risk of procedure-related complications. This report presents the results of the Multicentre European Radiofrequency Survey (MERFS) that was conducted by the Working Group on Arrhythmias of the European Society of Cardiology. The objectives of this voluntary retrospective survey were to assess the number of radiofrequency catheter ablation procedures performed in 86 European institutions from January 1987 until March 1992 and the incidence of procedure-related complications with respect to the different types of ablative procedures. A total of 4398 patients were reported on from 68 out of 86 institutions (79%) from 15 European countries that agreed to participate in MERFS. From 1987 to 1991, the number of patients who underwent RF ablation per year increased from 45 to 2000. In the first 3 months of 1992, a total of 1640 patients were reported on. The number of patients reported on in relation to the different types of ablative procedures were: ablation of atrial tachycardialatrial flutter: n = 141 (3.2%); ablation of the atrioventricular junction: n = 900 (20.5%); modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: n = 815 (18.5%); ablation of accessory pathway: n = 2222 (50.5%); ablation of ventricular tachycardia: n = 320 (7.3%). Procedure-related complications occurred in 223 patients (5.1%). The incidence of complications in relation to the ablative procedure was: ablation of atrial tachycardia/atrial flutter: 5.0%; ablation of the atrioventricular junction: 3.2%; modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: 8.0%; ablation of accessory pathway: 4.4%; ablation of ventricular tachycardia: 7.5%. Complications occurred significantly more often in patients who underwent modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia, when compared to ablation of the atrioventricular junction (P < 0.001) or ablation of accessory pathway (P < 0.001), and in patients who underwent ablation of ventricular tachycardia, when compared to ablation of the atrioventricular junction (P < 0.002) or ablation of accessory pathway (P < 0.02). The highest incidence of complications was reported after modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia.(ABSTRACT TRUNCATED AT 400 WORDS)

Trends in hospitalization for heart failure in Scotland 1980–1990

Abstract: Heart failure is a growing public health problem in industrialized countries with ageing populations. Scotland has a relatively stable population of approximately 5 million and a well described system for recording details of hospitalizations (Scottish Hospital In-Patients Statistics-SHIPS). We have examined SHIPS data for hospitalizations for heart failure in Scotland 1980–1990. Discharges for heart failure as the primary diagnosis increased by almost 60%, from 1.30 to 2.12/1000 population in this period (as either primary or secondary diagnosis the rate increased from 2.51 to 4.24/1000). Seventy-eight percent of discharges were in persons aged ≥ 65 years and 48% of discharges were male. Heart failure (primary diagnosis) accounted for almost 4% of all general (internal) medicine discharges. In-patient case fatality was 18% in 1990. Mean duration of in-patient stay on Internal Medicine wards was approximately 11 days. The number of hospitalizations for heart failure is now almost identical to those for myocardial infarction. These trends mirror those recently reported from the United States. Heart failure is an increasingly common and costly cause of hospitalization in Scotland. Approaches which can reduce this burden on the hospital service require urgent attention.

Evidence of oxidative stress in chronic heart failure in humans

Abstract: Chronic heart failure (CHF) due to coronary artery disease (CAD) has been shown to be associated with increased plasma thiobarbituric reactive substances (TBARS) and reduced plasma thiol (PSH) concentrations, suggesting oxidative stress (OS). The aims of the present studies were (a) to determine whether OS is due to CAD or CHF per se and (b) to determine if a wider range of more specific markers of OS are abnormal in CHF. In the first study, two groups of patients (n = 15 each) were compared. Group 1 (11 male, mean age 56 years) had CHF due to CAD and group 2 (12 male, mean age 53 years) had non-CAD CHF. Median plasma TBARS in controls was 7.6 nmol . ml−1 , 10.0 nmol . m−1 in group 1 and 9.3 nmol. ml−1 in group 2 ( P < 0.01 both groups vs control). Median PSH was 505 384 and 364 nmol. ml−1 ( P < 0.05 and P < 0.01 vs control) respectively. Fifty-three patients with CHF were recruited in the second study. Malondialdehyde and PSH were 10.3 and 409 nmol. ml−1 respectively, compared to control values of 7.9 and 560 nmol. ml.1 (both P < 0.001). The median values for the following additional measures of OS in controls and patients were: erythrocyte superoxide dismustase 131 vs 114 U . l−1 ( P = 0.005); caeruloplasmin oxidase 97 vs 197 U. l−1 ( P < 0.01); erythrocyte glutathione 1.56 nmol . ml−1 vs 1.77 nmol . ml−1 ( P < 0.02); plasma conjugated dienes 0.28 vs 0.33 optical density units ( P = ns). Chronic heart failure, regardless of aetiology, is associated with abnormalities of a range of markers of OS.

Platelet function, thrombin and fibrinolytic activity in patients with heart failure

Abstract: Assays which detect the release of platelet-specific proteins and of peptides during thrombogenesis and are considered markers of activation of platelets and the coagulation system have recently been developed. This study was designed to utilize these haemostasis-related markers to test the hypothesis that a prethrombotic state is related to the presence, aetiology and severity of heart failure. Seventy patients with heart failure were evaluated and data were compared with 36 normal volunteers and 41 patients with coronary artery disease without heart failure (CAD). Thrombogenesis was documented using assays which measure platelet function, thrombin activity and fibrinolysis. Platelet function was measured by determining plasma concentrations of platelet factor 4 (PF4) and beta-thromboglobulin (BTG). Thrombin-antithrombin III complexes (TAT) and fibrinopeptide A (FPA) were determined to evaluate thrombin activity. Fibrinolytic activity was assessed by measuring D-Dimer levels. Patients with heart failure, when compared to normals, had increased plasma levels of BTG (89 +/- 62 IU.ml-1 vs 50 +/- 59 IU.ml-1, P < 0.01), TAT (4.6 +/- 4.3 micrograms.l-1 vs 2.3 +/- 0.64 micrograms.l-1, P < 0.005), and D-Dimer levels (506 +/- 444 IU.ml-1 vs 191 +/- 144 IU.ml-1, P < 0.0001). Patients with heart failure, when compared to the CAD group, had increased plasma levels of D-Dimer (506 +/- 444 ng.ml-1 vs 191 +/- 144 ng.ml-1, P < 0.05). Aetiology of heart failure did not affect these measurements. Patients with severe heart failure, as determined by high plasma norepinephrine concentration or low ejection fraction, were more likely to have activation of platelets and the coagulation system.(ABSTRACT TRUNCATED AT 250 WORDS)

Cytomegalovirus and atherosclerosis.

Abstract: An avian herpesvirus is known to cause atherosclerosis in chickens The same virus can induce a proliferative disease, malignant lymphoma, suggesting that this agent may also have transforming potential and thus stimulate the proliferation of arterial smooth muscle cells, a prominent feature of atherogenesis The evidence for involvement of cytomegalovirus (CMV), a member of the human herpesvirus family, in atherosclerosis is much more circumstantial The finding of CMV antigen and nucleic acid sequences in arterial smooth muscle cells of humans suggests that viral infection of the arterial wall may be common in the general population, including patients with severe atherosclerosis In seroepidemiological studies, high levels of CMV antibodies were found to be associated with clinically manifest atherosclerotic disease, suggesting that a periodically activated latent infection or a continuously active infection is present in patients with atherosclerosis Since the viral genome but not infectious virus is found in arterial cells, the artery itself may be the site of CMV latency Of particular significance is the recent finding that heart transplant recipients, who are immunosuppressed, and who are also actively infected with CMV, are prone to develop accelerated atherosclerosis in the transplanted organ Although suggestive, these observations by themselves do not demonstrate that viruses have a role in the pathogenesis of atherosclerosis, but they support a working hypothesis of the steps involved

Long-term reduction of cardiac mortality after myocardial infarction : 10-year results of a comprehensive rehabilitation programme

Abstract: The long-term outcome of different methods of post-MI care has been studied in two non-selected groups of MI patients: an intervention group (n = 147), participating in a cardiac rehabilitation (CR) programme, was compared to a reference group receiving standard care (n = 158). The CR programme included a post-MI clinic, physical training, information on smoking and diet, and psychological support. After 5 years there was no difference in mortality (29.3 vs 31.6%), but the recurrence rate of non-fatal MI (17.3 vs 33.3%, P < 0.05) and of total cardiac events (39.5 vs 53.2%, P < 0.05) was lower in the intervention group, and more patients were still at work (51.8 vs 27.4% P < 0.01). After 10 years there was a reduction in total (42.2 vs 57.6% P < 0.01) and cardiac mortality (36.7 vs 48.1% P < 0.001). Fewer patients in the intervention group suffered from non-fatal reinfarction (28.6 vs 39.9%, P < 0.001). Among those patients who had not yet reached the age of retirement more patients had resumed employment (58.6 vs 22.0% P < 0.05). We conclude, that the secondary preventive effect of the programme has contributed to the higher rate of survival.

Diagnosis of heart tumours by transoesophageal echocardiography: a multicentre study in 154 patients

Abstract: In a retrospective multicentre study, the diagnostic potential of transoesophageal 2D-echocardiography (TEE) as compared to precordial 2D-echocardiography (TTE) was determined in 154 patients with primary or secondary tumours of the heart. Additionally, the value of standard diagnostic parameters, such as symptoms, X-ray of the chest and electrocardiogram were evaluated. In 84 patients (24 male, 60 female; age 20-85, mean 56.6 years) intracardial tumours were present, and 70 patients (37 male, 33 female; age 18-79, mean 44.3 years) presented with peri- or paracardial tumours. The main symptoms of patients with intracardial tumours were dyspnoea (60.7%), vena cava syndrome (22.2%) and chest pain (20.2%). Embolization was found in 11.9%. Left or right atrial enlargement was observed on chest X-ray in 23 patients, and echocardiographic abnormalities in 17 cases. The patients with peri- or paracardial tumours presented with dyspnoea in 51.4% of cases, loss in body weight in 20.0% and with vena cava syndrome and chest pain in 17.1%. The chest X-ray was abnormal in 56 patients. Unspecific ST segment changes in the electrocardiogram were observed in five, and arrhythmias in seven cases. Diagnosis of atrial myxomas was achieved by TTE in 95.2%, by TEE in 100%, by angiography in 78.4%, by computed tomography (CT) or magnetic resonance tomography (NMR) in 70%. Identification of the attachment point was made by angiography in 8.1%, by TTE in 64.5% and by TEE in 95.2%. In 22 patients with intracardial tumours (myxomas excepted) diagnosis was achieved by TTE in 90.9%, by TEE in 100%, by CT or NMR in 88.9% and by angiography in 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Methods for detection of left ventricular hypertrophy: application to hypertensive heart disease.

Abstract: Left ventricular hypertrophy (LVH) detected by electrocardiography (ECG) and, more recently, by echocardiography has been shown to be an extremely strong predictor of morbidity and mortality in patients with essential hypertension and in members of the general population. Increased left ventricular mass (LVM) is strongly related to both increased blood pressure and overweight. Indexation of LVM by body surface or height has advantages for the detection of LVH related to hypertension or obesity. Indexation of LVM for height to the power 2.7 revealed by analysis of growth (allometric) relations may accomplish both these goals. In validation studies, the sensitivity of echocardiography to detect LVH has been reasonably high (85-100%), whereas that of ECG has ranged from as high as 50% in severely diseased necropsy populations to as low as 6-17% in recent studies in Cornell and Framingham. ECG sensitivity can be improved by using Cornell multivariate regression equations or by consideration of the Cornell voltage-QRS duration product. Obesity dramatically decreases the sensitivity of the ECG for detection of LVH, and recent research suggests a lower specificity and a higher rate of false-positive ECG diagnoses of LVH in black than in white subjects. Standard criteria for ECG LVH are less useful than echocardiographic findings for stratifying populations into high- and low-risk subgroups because of lower sensitivity, but improved ECG criteria need further evaluation in this respect.

Missing teeth and ischaemic heart disease in men aged 45-64 years.

Abstract: The aim of the present study was to investigate the associations between number of missing teeth (expressing sustained oral infections) and diagnosed ischaemic heart disease using cross-sectional data from 1384 men aged 45-64 years. The study population was derived from a representative sample of adult Finns. Ischaemic heart disease was considered to be present in those with angina pectoris or previous myocardial infarction, whether definite or possible. A tooth was recorded as missing if none of it was visible or could be felt with an instrument. According to multiple linear analyses, the variation in ischaemic heart disease was independently explained by age, clinical diagnosis of arterial hypertension, geographical area, educational level and number of missing teeth. Smoking and cholesterol were not significant explanatory factors. The explanation for the observed association between missing teeth and ischaemic heart disease is that they may share a common behavioural background factor. There may also be a more direct causal relationship between the phenomena.

Pathogenetic mechanisms and epidemiology of Chlamydia pneumoniae.

Abstract: The antibody prevalence data indicate that C. pneumoniae infections are common worldwide and more frequently occur in middle-aged and elderly males than in females. C. pneumoniae infections are first acquired in childhood in heavily populated areas, whereas in northern countries, first infections are generally at teenage and in Scandinavia, typically at the time of military service. All chlamydial species tend to cause chronic infections, with severe sequelae developing 10 to 50 years after the primary infections. If C. pneumoniae resides in alveolar macrophages or in vascular endothelial cells in chronic infections the bacteria and their structural components, such as lipopolysaccharides have an easy access to circulation. The continuous induction of cytokines by C. pneumoniae may lead to chronic inflammation of vascular endothelium.

Comparison of flecainide and procainamide in cardioversion of atrial fibrillation.

Abstract: In this prospective, controlled and randomized cross-over study we tried to establish the efficiency and safety of flecainide vs procainamide for the treatment of acute atrial fibrillation. Eighty patients (30 females, 50 males, mean age: 55 +/- 14 years) were included. Patients entered into the study if they had atrial fibrillation of recent onset ( 100 beats.min-1 at rest and were < 75 years of age. Exclusion criteria were any sign of heart failure, conduction disturbances, sick sinus syndrome or acute ischaemic events. Randomly 40 patients received flecainide and 40 procainamide as the first treatment. There were no significant clinical difference between the two groups. Procainamide ws given at a dose of 1 g infused over 30 min, and followed by an infusion of 2 mg.min-1 over 1 h. Flecainide was given at a dose of 1.5 mg.kg-1 over 15 min followed by an infusion of 1.5 mg.kg-1 over 1 h. Drug infusion was continued until maximal dose, intolerance or reversion to sinus rhythm. After 1 h of wash out, patients remaining in atrial fibrillation were started on the second drug. Left atrial size was measured by echo. Serum levels of drug and atrial size did not differ between patients who returned to sinus rhythm and those who remained in atrial fibrillation. Conversion to sinus rhythm was achieved in 37 (92%) of the 40 patients treated with flecainide and 25 (65%) of those treated with procainamide (P < 0.001). The time required for reversion to sinus rhythm was similar between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial damage during ischaemia and reperfusion

Abstract: Reperfusion, without doubt, is the most effective way to treat the ischaemic myocardium. Late reperfusion may, however, cause further damage. We attempted to identify the nature and time-course of metabolic changes occurring during ischaemia followed by reperfusion either in isolated and perfused rabbit hearts or in coronary artery disease (CAD) patients undergoing intracoronary thrombolysis or aortocoronary bypass grafting. In isolated hearts, reperfusion after prolonged ischaemia causes exacerbation of cell damage, leading to a breakdown of the permeability barrier of ions as well as of larger molecules, such as creatine phosphokinase. As consequence, reperfusion results in a large increase in intracellular calcium, leading to mitochondrial calcium overload with subsequent damage to the mitochondrial structure and loss of the ability to produce adenosine triphosphate (ATP). The ultimate mediator of the membrane damage is not known. It has been suggested that myocardial production of oxygen free radicals above the neutralizing capacity of the myocytes is an important cause of reperfusion damage. There is evidence that prolonged ischaemia reduces the naturally occurring defence mechanisms of the heart against oxygen free radicals, particularly mitochondrial manganese superoxide dismutase, and the intracellular pool of reduced glutathione. Consequently, reperfusion results in severe oxidative damage, as evidenced by tissue accumulation and release of oxidized glutathione. An oxygen free radical-mediated impairment of mechanical function also occurs during reperfusion of the human heart. During surgical reperfusion of CAD patients, we observed a prolonged and sustained release of oxidized glutathione; the degree of oxidative stress can inversely correlated with recovery of mechanical and haemodynamic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Rheumatic heart disease in the developing world: prevalence, prevention, and control

Abstract: Rheumatic heart disease (RHD) continues to be a common health problem in the developing world, causing morbidity and mortality among both children and adults. Although little longitudinal data are available, evidence suggests that there has been little if any decline in the occurrence of RHD over the past few decades. Recent reports from the developing world have documented rheumatic fever (RF) incidence rates as high as 206/100,000 and RHD prevalence rates as high as 18.6/1000. The high frequency of RHD in the developing world necessitates aggressive prevention and control measures. The major interventions for prevention and control include: (1) reduction of exposure to group A streptococci, (2) primary prophylaxis to prevent initial episodes of RF, and (3) secondary prophylaxis to prevent recurrent episodes of RF. Because recurrent episodes of RF cause increasingly severe cardiac complications, secondary prophylaxis is the most crucial feature of an effective RHD programme. For some impoverished countries, secondary prophylaxis may be the only intervention that can realistically be implemented. In addition to this intervention, however, financial and human resources must be committed, and all of these elements must be integrated into existing primary health care systems. Because RHD continues to be a common health problem in the developing world, greater emphasis needs to be placed on the simple and cost-effective prevention and control measures that are currently available to combat this disabling disease.

Antiarrhythmic drugs and torsade de pointes.

Abstract: In the past decade there has been much progress in understanding the clinical features and associations of drug-induced long QT syndromes, their inter-relationships with other long QT syndromes, and electrophysiological mechanisms that may be involved in the development of torsade de pointes, the major proarrhythmic correlate of prolonged repolarization. The most likely electrophysiologic basis for torsade de pointes is the development of after-depolarizations facilitated by hypokalemia, bradycardia and lengthened QT intervals. Torsade de pointes can be produced by all antiarrhythmic agents that lengthen repolarization, although the precise incidence varies with different agents and is not quantitatively related to the degree of QT prolongation. Quinidine, disopyramide and procainamide (with its metabolite N-acetyl procainamide) are strongly concordant in the production of torsade de pointes. Such concordance suggests that there is an individual predisposition to the induction of early after-depolarizations (EAD) with exposure to agents that prolong repolarization. However, concordance with agents or other classes, such as sotalol, is less certain, and amiodarone appears to be discordant. The discordance between potency in prolonging the QT interval and the proclivity to induce torsade de pointes may hold the key to separating the salutary therapeutic antiarrhythmic effects from adverse proarrhythmic effects of class III agents. There is an optimistic perception that the development of new agents that potently prolong repolarization will give a modern realization of the old concept that prolongation of refractoriness is a uniquely powerful anti-re-entrant, antitachyarrhythmic action.

Evidence for biventricular involvement in acromegaly: a Doppler echocardiographic study

Abstract: To investigate left and right ventricular involvement in acromegaly, 20 patients were studied by Doppler echocardiography. Nine of them had systemic hypertension. Right ventricular free wall thickness was significantly increased in acromegalic patients (8 +/- 2 vs 4 +/- 1 mm; P < 0.001). Left ventricular mass index was augmented both in the whole group and in the subgroup of normotensive acromegalics, as compared with normals (134 +/- 33 and 115 +/- 20 vs 80 +/- 18 g.m-2; P < 0.01). Ejection phase indices were normal in the patient group, while impaired left and right ventricular diastolic filling was found. In fact isovolumic relaxation time was prolonged (118 +/- 21 vs 78 +/- 12 ms; P < 0.001), ratio of early to late mitral (0.9 +/- 0.3 vs 1.8 +/- 0.5; P < 0.001) and tricuspid (1.0 +/- 0.2 vs 1.4 +/- 0.3; P < 0.001) flow velocities were significantly decreased as compared with controls. Superior vena cava flowmetry was also abnormal showing a marked decrease of diastolic filling wave and, consequently, of the ratio between peak diastolic and peak systolic flow velocity. No significant differences were observed between normotensive and hypertensive acromegalics, except for left ventricular mass index (115 +/- 20 vs 156 +/- 31 g.m-2; P < 0.01). These findings indicate that abnormal diastolic filling patterns of transmitral, transtricuspid, and superior vena cava flowmetry suggesting 'impaired relaxation' associated with increased left and right ventricular mass, frequently occur in acromegaly.

A mechanism of cardiac pain suppression by spinal cord stimulation: implications for patients with angina pectoris

Abstract: Clinical reports show that electrical stimulation of the spinal cord reduces symptoms of angina pectoris, but so far have not provided evidence on the mechanisms involved. The hypothesis for this study was that inhibition of spinothalamic tract transmission may account for this result. Extracellular potentials of 28 spinothalamic tract neurons were recorded in anaesthetized monkeys, and the effects of dorsal column stimulation were determined on activity evoked by cardiac and somatic stimuli. Dorsal column stimulation reduced the number of cell potentials evoked by electrical stimulation of cardiopulmonary sympathetic afferent fibres in 11 spinothalamic tract cells tested. Activity evoked by intracardiac injection of bradykinin was decreased by dorsal column stimulation in six of seven neurons that responded to chemical stimulation of afferents. Differential effects of dorsal column stimulation were correlated to the cell responses to somatic field stimulation. Dorsal column stimulation inhibited activity in 12 of 12 neurons which were excited only by noxious pinch of somatic fields, whereas eight of 16 neurons which were excited by innocuous brushing of somatic fields were unaffected or excited. Transection of the dorsal column showed that the pathway transmitting inhibitory impulses descended from the stimulation site to the spinothalamic tract neurons examined. Results of this study are consistent with the concept that spinal cord stimulation reduces pain by decreasing the firing of spinothalamic tract cells which are activated by small fibre afferents. The paresthesias associated with nerve stimulation techniques may result from activation of spinothalamic tract cells which are excited by large fibre afferents. The clinical decision to employ spinal cord stimulation in patients with angina should balance the obvious benefit of pain relief against the risk of depriving the patient of an important warning signal while active myocardial ischaemia is in progress.

Dental infections as a risk factor for acute myocardial infarction.

Abstract: The so-called classic risk factors of coronary heart disease (CHD) do not explain all its clinical and epidemiological features. Recent evidence suggests that certain infections, among them dental infections, are involved in the pathogenesis of CHD. Case-control studies have revealed an association between dental infections and acute myocardial infarction and chronic coronary heart disease. A large epidemiological survey revealed an association between missing teeth and CHD and a recent 14-year follow-up of 9760 individuals showed that periodontitis is associated with an increased risk of coronary heart disease. Preliminary results suggest that the severity of dental infections correlates with the extent of coronary atheromatosis. Individuals with severe dental infections also have higher level of von Willebrand factor antigen, leukocytes and fibrinogen. Streptococcus sanguis has been shown to aggregate human platelets in vitro. The mechanism behind the association between dental infections and CHD could be the effect of bacteria on the cells taking part in the pathogenesis of atherosclerosis and arterial thrombosis.

Subjective symptoms and well-being differ in women and men after myocardial infarction

Abstract: The frequency of subjective cardiac and psychological complaints among men and women a year after a confirmed diagnosis of myocardial infarction (MI) were compared. Among 660 survivors, 595 patient ...

Serum C-reactive protein and infarct size in myocardial infarct patients with a closed versus an open infarct-related coronary artery after thrombolytic therapy

Abstract: Serum C-reactive protein rises in acute myocardial infarction, correlating positively with infarct size if thrombolytic treatment is not given. This correlation disappears if thrombolytic treatment is given, although the serum C-reactive protein concentration is still associated with the clinical outcome of the patient. We studied the effect of early coronary recanalization induced by thrombolytic treatment alone or combined with coronary angioplasty on the infarct related rise in serum C-reactive protein concentration. The C-reactive protein response caused by the myocardial infarct was lower in patients with an open infarct-related coronary artery than in patients with a closed infarct-related coronary artery, or in control patients who did not receive thrombolytic therapy. In control patients we found the expected strong positive correlation between infarct size and serum C-reactive protein (r = 0.58; P < 0.001, n = 48), which was similar to that in patients with a closed infarct-related coronary artery (r = 0.62; P < 0.001, n = 17). In patients with an open infarct-related coronary artery the correlation between infarct size and serum C-reactive protein was much weaker (r = 30; P < 0.01, n = 91). Consequently infarct size explained approximately 35% of the variation in serum C-reactive protein values in the control patients and 36% in the patients with a closed infarct-related coronary artery, but only 9% of the variation in the patients with an open infarct-related artery. Ejection fraction correlated negatively with serum C-reactive protein in both control and recanalized patients. The association was again much stronger in the control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Novel actions of methylene blue.

Abstract: Methylene blue has been frequently used as an inhibitor of soluble guanylyl cyclase. We found that endothelium-dependent relaxations of isolated blood vessels were considerably more sensitive to inhibition by methylene blue than relaxation induced by direct activators of soluble guanylyl cyclase. Similar data were obtained in the presence of superoxide dismutase, indicating that the diverse potencies of methylene blue were not due to superoxide-induced inactivation of nitric oxide (NO). Subsequent experiments revealed that methylene blue is an inhibitor of purified NO synthase. Conversion of L-arginine to L-citrulline was inhibited by the dye in a concentration-dependent fashion with half-maximal effects observed at 5.3 microM and 9.2 microM in the absence and presence of superoxide dismutase, respectively. Purified soluble guanylyl cyclase, however, was far less sensitive to methylene blue. When the enzyme was maximally stimulated with S-nitroso-glutathione, cyclic guanosine monophosphate, (cGMP) formation was reduced by 50% at approximately 60 microM methylene blue; 1 mM produced maximal inhibitions of about 70%. Our data indicate that methylene blue is only a poor inhibitor of soluble guanylyl cyclase. The dye seems to act primarily via inhibition of NO synthase, with enzyme-bound heme being a possible target in its inhibitory action.

Regional wall motion abnormalities in stunned and hibernating myocardium.

Abstract: The clinical recognition that chronic dysfunctioning myocardial segments may retain viable myocardium has important therapeutic consequences. ‘Stunned myocardium’ and ‘hibernating myocardium’ have been proposed to distinguish respectively between post-ischaemic left ventricular dysfunction, a condition which normalizes spontaneously, and persistent wall motion abnormalities due to chronic hypoperfusion. This study examines the possible link between these two conditions.

Infection and inflammation as risk factors for myocardial infarction.

Abstract: Recent studies have illustrated that in addition to the well known risk factors, such as lipoproteins, smoking, hypertension, there are others that cause atherosclerosis and myocardial infarction. Our knowledge of atherosclerotic lesions has increased. We now know that atherosclerotic changes are due to inflammatory cell infiltration as well as to increases in migration of vascular smooth muscle cells. Endothelial cells play a major role in the pathology of vascular changes. In recent years a new risk factor for coronary artery disease has been discovered: chlamydia pneumonial infections. Herpes class viruses have also been associated with pathology of atherosclerotic lesions. Studies show that dental status and bacterial infections are also related to the risk of myocardial infarction. This review discusses the possible mechanisms of infection and inflammation and whether they are major or modifying risk factors for atherosclerosis and myocardial infarction.

Quantitation of global and regional left ventricular function by cine magnetic resonance imaging during dobutamine stress in normal human subjects

Abstract: Magnetic resonance imaging (MRI) provides high-resolution images of the heart. However, physical exercise during MRI is difficult due to space restriction and motion artefacts. To evaluate the feasibility of MRI during stress conditions, dobutamine was used as an alternative to exercise. Haemodynamics, ventricular volumes and wall thickening were measured at rest and during peak dobutamine infusion (15 micrograms.kg-1 x min-1) in 23 normal human subjects. To calculate left ventricular volumes, eight short-axis views were obtained encompassing the left ventricle from base to apex. At six levels, percent systolic wall thickening (%WTh) was measured in 18 segments (20 degrees intervals). Heart rate, systolic and diastolic blood pressures, stroke index, cardiac output and left ventricular ejection fraction increased significantly during dobutamine infusion (all P values < 0.001). In addition, %WTh increased significantly (P < 0.001) during dobutamine compared to the control state at all levels except in the apical and low-left ventricular levels. Both in control conditions and during dobutamine, segmental wall motion analysis showed the highest %WTh at the posterolateral area and the lowest %WTh at the septal region (P < 0.05). MRI clearly identifies wall motion dynamics and provides calculations of segmental wall thickening and haemodynamic parameters. Dobutamine is a useful stress agent by virtue of its safety, operator control and its effects which resemble physical exercise.

Isoforms of nitric oxide synthase: functions in the cardiovascular system.

Abstract: Various cell types, including endothelial cells, can synthesize nitric oxide (NO). Three different isoforms of NO synthase have been characterized, purified and cloned. Isozyme I is present in neuronal cells of the brain (where NO may mediate synaptic plasticity), in peripheral non-adrenergic non-cholinergic (NANC) neurons (where NO acts as an atypical neurotransmitter relaxing vascular and non-vascular smooth muscle), and in various specialized epithelial cells. Macrophages can be induced with bacterial endotoxin and/or cytokines to express isozyme II. The high concentrations of NO produced by this isoform have cytostatic effects on parasitic microorganisms and tumour cells. A similar isozyme can be induced in the vascular wall (presumably in smooth muscle cells) in sepsis and during cytokine therapy. The large amounts of NO produced by this enzyme contribute to the symptoms of septic shock, such as vasodilatation and microvascular endothelial damage. Endothelial cells contain isoform III of NO synthase which seems to be unique for this cell type. Endothelium-derived NO is a physiologically significant vasodilator and inhibitor of platelet aggregation and adhesion. In addition, vascular NO can prevent leukocyte adhesion to the endothelium by interfering with the adhesion molecule CD11/CD18, and NO has also been shown to inhibit the proliferation of vascular smooth muscle cells. Hence, NO represents a protective factor against vascular damage and probably atherogenesis.

Intra-aortic balloon counterpulsation improves survival in cardiogenic shock complicating acute myocardial infarction

Abstract: The impact of intra-aortic balloon counterpulsation (IABC) on survival of patients with acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) has been evaluated in this study of 85 patients. IABC was available for the 24 group A patients (and used in 20 patients). IABC was not available for the 21 group B patients who presented simultaneously with similar clinical characteristics and received identical pharmacological treatment. In-hospital and one year survival was significantly higher in group A (46% and 38% vs 19% and 10%, P < 0.001). Sixteen out of the 20 (group A1) IABC patients received early coronary revascularization. During 1980-1984, 35 patients with AMI and CS received IABC (group C) but none underwent early revascularization. There was no difference in in-hospital or one-year survival between group A1 (50% and 40%) and group C (45% and 40%). We conclude that early IABC improves survival of patients with AMI complicated by CS.

Enhanced sensitivity for detection of coronary artery disease by addition of atropine to dipyridamole echocardiography

Abstract: Dipyridamole echocardiography test (DET) has gained acceptance due to its safety, feasibility, diagnostic accuracy and prognostic power. The main limitation of the test is a less than ideal sensitivity in some patient subsets, such as those with limited coronary artery disease. Atropine with dipyridamole might theoretically combine to become a synergistic ischaemic stress test, by increasing myocardial oxygen demand through chronotropic stress and by reducing flow supply through a shortening of the diastolic interval under maximal coronary vasodilation. The aim of this study was to assess the effects of the addition of atropine to DET. Three hundred and twenty-one patients (age = 58 +/- 9 years), referred for testing in the echo lab, were initially studied by DET. Of these, 151 were stopped during or within the 2 min following dipyridamole infusion because of achievement of a predetermined end-point: obvious echocardiographic positivity (n = 137), severe chest pain (n = 3), diagnostic ST segment changes (n = 7) or limited side effects (n = 4). In another three cases, atropine was not given due to a history of glaucoma or severe prostatic hypertrophy. In the remaining 167 patients with a negative DET test, atropine (0.25 mg intravenously, repeated every min up to a maximum of 1 mg, if necessary) was added, starting 3 min after the end of the dipyridamole infusion. The dipyridamole-atropine echo test (DETA) was positive in 32 and negative in 135 patients, and no major side effects occurred in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Polycystic disease of the kidneys complicating the diagnosis of myocardial echinococcosis

Abstract: The case of a 30-year-old woman with polycystic disease of the kidneys and a large cyst in the interventricular septum is presented. The hypothesis of an echinococcal disease or of a cardiac manifestation of a polycystic disease was raised. The patient's history, serologic data, and the morphological aspect of the cyst did not give evidence for echinococcal disease before surgery. However, the postoperative pathological evaluation confirmed the diagnosis of a single echinococcal cyst. The presented case shows that even in cases without proven diagnosis of echinococcal disease and preexisting hereditary cysts in other organ systems, care should be taken during surgery to avoid anaphylaxis and preoperative spread of the parasite throughout the body.

The influence of intravenous magnesium sulphate on the occurrence of atrial fibrillation after coronary artery by-pass operation

Abstract: To examine the influence of magnesium (Mg) on hypomagnesaemia and atrial fibrillation (AF) following coronary artery by-pass surgery, 140 consecutive patients were randomized to receive 70 mmol of magnesium sulphate intravenously (n = 69) or placebo (n = 71). Serum magnesium concentrations fell to 0.77 +/- 0.10 mmol.l-1 in the control group but rose to 1.09 +/- 0.17 mmol.l-1 in the Mg group (P < 0.001). The incidence of AF was 29% in the Mg group and 26% in the placebo group (NS). The AF patients were older, more of them had had prior AF episodes, their sinus rates (SR) were slower (78 +/- 10 vs 86 +/- 12 beats.min-1; P < 0.01) and serum Mg concentrations higher (0.89 +/- 0.21 vs 0.80 +/- 0.11 mmol.l-1; P < 0.05). The incidence of AF was 43% in the highest quartile of serum Mg and 23% among the rest (P = 0.056). In patients experiencing AF during the first three post-operative days, serum Mg concentrations were higher and SR slower on each day compared with non-AF patients. SR increased post-operatively less with high Mg levels (P = 0.044). In the Mg group, serum Mg and SR were the only independent predictors of AF. In conclusion, the incidence of post-operative AF is not decreased with magnesium. High Mg levels are likely to provoke AF probably by mechanisms that modify SR.

Biotransformation to nitric oxide of organic nitrates in comparison to other nitrovasodilators

Abstract: Nitrovasodilators are prodrugs which, although chemically heterogenous, exert their pharmacodynamic action via a common pathway, i.e. the release of nitric oxide (NO). The NO, which results from metabolism of nitrovasodilators in vascular and non-vascular cells, stimulates the cytosolic enzyme guanylyl cyclase leading to an increase in the concentration of intracellular cyclic guanosine monophosphate (cGMP). In general, the rate of NO generation from the individual compounds correlates well with the extent of cGMP increase and their potency to relax vascular tissue. The amounts of NO generated are sufficient to inhibit platelet aggregation and to induce disaggregation. Nitrovasodilators thus mimic the action of endothelium-derived relaxing factor (EDRF). After more than a century of empiric use, the application of nitrovasodilators today may be regarded as causal therapy, since these drugs act by substituting an endogenous factor, the production or release of which is impaired under pathophysiological circumstances associated with endothelial dysfunction. Marked differences exist between individual compound classes with regard to bioactivation mechanisms, cofactor requirements, and the extent and nature of the concomittant formation of metabolites other than NO. This review describes the discovery of the mode of action of nitrovasodilators and our current understanding of the pathways involved in their bioactivation and biodegradation with special emphasis on the enzymatic and non-enzymatic metabolism of organic nitrates. In addition, the in-vivo metabolism of NO is reviewed briefly