Search PubMed⌕ Search

Biomedical subjects

M Stramba-Badiale

Publications and source records attributed to M Stramba-Badiale.

At least 37 records · Page 2Linked to original sources
PubMed1991

Vagal reflexes and survival during acute myocardial ischemia in conscious dogs with healed myocardial infarction.

The role of vagal tone and reflexes in the genesis of life-threatening arrhythmias was investigated in a clinically relevant animal model for sudden cardiac death. Forty-five dogs with a healed anterior myocardial infarction in which transient myocardial ischemia during exercise did not induce malignant arrhythmias were utilized for the study. They underwent a further exercise and ischemia test in which atropine (75 micrograms/kg) was injected before coronary artery occlusion. Novel occurrence of ventricular arrhythmia, or worsening of the type of arrhythmia present in the control test, occurred in 23 of 45 dogs (51%) and ventricular fibrillation occurred in 11 of 45 (24%, P = 0.001). Analysis of heart rate response to acute ischemia in the control test indicates that these 11 animals had powerful vagal reflexes during coronary artery occlusion, compared with the 34 survivors (-32 +/- 35 vs. +2 +/- 27 beats/min, P = 0.003). This study indicates that approximately 75% of animals resistant to ventricular fibrillation are characterized by weak sympathetic reflexes in response to acute myocardial ischemia. In the remaining 25% powerful vagal reflexes counteract concomitant reflex sympathetic hyperactivity, decrease heart rate, and are essential for survival.

Acute Disease↗
PubMed1991

Unsuspected echocardiographic abnormality in the long QT syndrome. Diagnostic, prognostic, and pathogenetic implications.

BACKGROUND: The idiopathic long QT syndrome (LQTS) is characterized by electrocardiographic abnormalities and by a high incidence of lethal arrhythmias. The present case/control study demonstrates the frequent occurrence of unusual and specific ventricular wall motion abnormalities in LQTS and their association with history of syncope or cardiac arrest. These anomalies were present in 23 of 42 LQTS patients (55%) and in two of 42 healthy controls (5%, p less than 0.0001) matched for age, sex, height, and weight. METHODS AND RESULTS: Two new measurements were developed to assess quantitatively the abnormalities observed. The first, Th1/2, is an index of the rapidity of the early contraction phase; the second, TSTh, is an index of the presence of a slow movement in the late thickening phase. Th1/2 was smaller in LQTS patients (15.0 +/- 4.1 versus 19.9 +/- 3.9% of the cardiac cycle, p less than 0.001), indicating that they reach half-maximal systolic contraction more rapidly than controls. TSTh was greater in LQTS patients (9.37 +/- 6.82 versus 2.88 +/- 4.46%, p less than 0.001), indicating that they spend more time at a very low thickening rate. A peculiar double peak pattern of late thickening was present in 11 patients and in no controls. These abnormalities were more frequent in symptomatic than in asymptomatic patients (20 of 26, 77%, versus three of 16, 19%, p less than 0.005; relative risk, 2.75). They were not affected by beta-blockade or by left cardiac sympathetic denervation. The same echocardiographic abnormalities were produced by right stellectomy in nine of nine anesthetized dogs, were not dependent on cycle length, and were not modified by subsequent left stellectomy. CONCLUSIONS: This study demonstrates a previously unsuspected abnormality in the ventricular contraction pattern of LQTS patients and, for the first time, provides evidence that a noninvasively detected cardiac abnormality is associated with a higher risk for syncope/cardiac arrest. The experimental reproduction of this echocardiographic abnormality by right stellectomy indicates that this newly found clinical characteristic of LQTS does not contradict the "sympathetic imbalance" hypothesis.

Adult↗
PubMed1991

Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction.

The interest for the antifibrillatory effect of vagal stimulation has been largely limited by the fact that this concept seemed restricted to acute experiments in anesthetized animals. To explore the potentially protective role of vagal stimulation in conscious animals we developed a chronically implantable device to be placed around the cervical right vagus. An anterior myocardial infarction was produced in 161 dogs; 1 month later an exercise stress test was performed on the 105 survivors. Toward the end of the test the circumflex coronary artery was occluded for 2 minutes. Fifty-nine (56%) dogs developed ventricular fibrillation and, before this test was repeated, were assigned either to a control group (n = 24) or to be instrumented with the vagal device (n = 35). Five dogs were excluded because of electrode malfunction. Compared with the heart rate level attained after 30 seconds of occlusion during exercise in the control test, vagal stimulation led to a decrease of approximately 75 beats/min (from 255 +/- 33 to 170 +/- 36 beats/min, p less than 0.001). In the control group 22 (92%) of 24 dogs developed ventricular fibrillation during the second exercise and ischemia test. By contrast, during vagal stimulation ventricular fibrillation occurred in only 3 (10%) of the 30 dogs tested and recurred in 26 (87%) during an additional exercise and ischemia test in the control condition (p less than 0.001 versus the vagal stimulation test; internal control analysis). Combined analysis of the tests performed in the control condition showed that ventricular fibrillation was reproducible in 48 (89%) of the 54 dogs tested. The protective effect of vagal stimulation was also significant in the group comparison analysis and even after exclusion of those four dogs in which ventricular fibrillation was not reproducible (92% versus 11.5%, control versus vagal stimulation, p less than 0.001). When heart rate was kept constant by atrial pacing, the vagally mediated protection was still significant (p = 0.015) as five (55%) of nine dogs survived the test. This study shows that vagal stimulation, performed shortly after the onset of an acute ischemic episode in conscious animals with a healed myocardial infarction, can effectively prevent ventricular fibrillation. This striking result seems to depend on multiple mechanisms having a synergistic action. The decrease in heart rate is an important but not always essential protective mechanism. The electrophysiological effects secondary to the vagally mediated antagonism of the sympathetic activity on the heart are likely to play a major role.

Animals↗
PubMed1990

Heart rate variability before and after myocardial infarction in conscious dogs at high and low risk of sudden death.

Heart rate variability has been demonstrated both experimentally and clinically to be of prognostic importance in determining mortality after myocardial infarction. However, no paired studies have been reported to examine heart rate variability before and after myocardial infarction. The hypothesis was tested that low values of heart rate variability provided risk assessment both before and after myocardial infarction with use of an established canine model of sudden cardiac death. Risk for sudden death was assessed 1 month after myocardial infarction by a protocol in which exercise and myocardial ischemia were combined; dogs that developed ventricular fibrillation were classified at high risk for sudden death (susceptible) and the survivors were considered low risk (resistant). In resistant dogs, myocardial infarction did not affect any measure of heart rate variability: 1) mean RR interval, 2) standard deviation of the mean RR interval, and 3) the coefficient of variance (standard deviation/RR interval). By contrast, after myocardial infarction, susceptible dogs showed significant decrease in all measures of heart rate variability. Before myocardial infarction, no differences were seen between susceptible and resistant dogs. However, 30 days after infarction, epidemiologic analysis of the coefficient of variance showed high sensitivity and specificity (88% and 80%, respectively), predicting susceptibility. Therefore, results of analysis of 30 min of beat to beat heart period at rest 30 days after myocardial infarction are highly predictive for increased risk of sudden death.

Analysis of Variance↗
PubMed1990

Carbon monoxide and lethal arrhythmias.

The effect of acute exposure to carbon monoxide on ventricular arrhythmias was studied in a previously described chronically maintained animal model of sudden cardiac death. In 60 percent of dogs with a healed anterior myocardial infarction, the combination of mild exercise and acute myocardial ischemia induces ventricular fibrillation. The events in this model are highly reproducible, thus allowing study by internal control analysis. Dogs that develop ventricular fibrillation during the test of exercise and acute myocardial ischemia are considered at high risk for sudden death and are defined as "susceptible"; dogs that survive the test without a fatal arrhythmia are considered at low risk for sudden death and are defined as "resistant." In the current study, the effects of carboxyhemoglobin levels ranging from 5 to 15 percent were tested in resistant and susceptible dogs. A trend toward higher heart rates was observed at all levels of carboxyhemoglobin, although significant differences were observed only with 15 percent carboxyhemoglobin. This trend was observed at rest and during exercise in both resistant and susceptible dogs. In resistant animals, in which acute myocardial ischemia is typically associated with bradycardia even under the control condition, this reflex response occurred earlier and was augmented after exposure to carbon monoxide. This effect may depend on the increased hypoxic challenge caused by carbon monoxide, and thus on an augmentation of the neural reflex activation or a sensitization of the sinus node to acetylcholine induced by hypoxia. In both resistant and susceptible dogs, carbon monoxide exposure induced a worsening of ventricular arrhythmias in a minority of cases. This worsening was not reproducible in subsequent trials. These data indicate that acute exposure to carbon monoxide is seldom arrhythmogenic in dogs that have survived myocardial infarction. Nevertheless, the observation that carbon monoxide exposure increases heart rate at rest and during moderate exercise may have clinical implications relevant to patients with coronary artery disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMed1989

Carbon monoxide and lethal arrhythmias in conscious dogs with a healed myocardial infarction.

Environmental studies suggested that exposure to carbon monoxide (CO) increases cardiovascular mortality among patients with coronary artery disease. We investigated whether, in dogs with a healed anterior myocardial infarction at low and high risk for ventricular fibrillation, acute exposure to CO has adverse effects during acute myocardial ischemia combined with exercise. One month after myocardial infarction, 17 dogs had ventricular fibrillation and 16 survived during the combined exercise and ischemia test. These tests were then repeated in all dogs with different concentrations of carboxyhemoglobin (COHb) (from 5% to 15%). With 15% COHb, heart rate (HR) at rest and during exercise was higher (p less than 0.05) than in the control tests. Surprisingly, the reflex HR response to acute ischemia was also altered; namely, the HR reduction characteristic of the low-risk animals was anticipated and accentuated (-31 +/- 25 versus 2 +/- 30 beats/min, p less than 0.05). Conversely, the HR increase characteristic of the high-risk group was reduced by CO (44 +/- 52 versus 72 +/- 43 beats/min, p less than 0.05). With 15% COHb, malignant arrhythmias occurred in two of the low-risk dogs and in none of the high-risk dogs. In the latter, CO was tested with a combination of exercise work load and myocardial ischemia duration not associated with ventricular fibrillation (VF) in the control condition. This study demonstrated that brief exposure to CO (1) profoundly alters the reflex HR response to exercise and to acute myocardial ischemia and (2) does not enhance the occurrence of malignant arrhythmias in conscious dogs with a healed myocardial infarction.

Animals↗
PubMed1988

Response of cytochrome a,a3 to carbon monoxide in canine hearts with prior infarcts.

The effects of moderate levels of carbon monoxide (CO) on the oxidation-reduction state of cytochrome a,a3 (cyt a,a3) were examined in the hearts of twelve dogs with a prior myocardial infarction. Exposure to ten minutes CO produced a carboxyhemoglobin (CO-Hb) level of 9.4%, a level experienced by heavy smokers. Accompanying the exposure to CO, cyt a,a3 became more reduced; 17.4% +/- 4.7%. Exposure to CO was accompanied by an increase of 33% +/- 4% in the rate of cyt a,a3 reduction following occlusion of the left circumflex coronary artery and a decrease of 24% +/- 8% in the rate of cyt a,a3 oxidation with release. There was also a decrease in the magnitude of cyt a,a3 reduction from 86% +/- 9% to 70% +/- 11%. These results indicate that moderate levels of CO trap cyt a,a3 in the reduced state which impairs the ability of the heart to recover from transient ischemic episodes.

Animals↗
PubMed1988

Autonomic mechanisms and sudden death. New insights from analysis of baroreceptor reflexes in conscious dogs with and without a myocardial infarction.

We have suggested that among conscious dogs with a healed anterior wall myocardial infarction (MI) a depressed baroreflex sensitivity (BRS) carries a higher risk of developing ventricular fibrillation during a brief ischemic episode associated with an exercise stress test. The clinical and pathophysiological implications of our previous findings prompted the present study, which addressed three major questions: 1) Is, indeed, analysis of BRS after MI a specific and sensitive marker for sudden death-risk stratification? 2) Does MI modify BRS? 3) Does analysis of BRS before MI provide information about outcome during ischemic episodes occurring after MI? An anterior MI was produced in 301 dogs, and 4 weeks later, a 2-minute circumflex coronary artery occlusion beginning during the last minute of an exercise stress test could be performed in 192 animals. Ventricular fibrillation occurred in 106 (55%) dogs (susceptible to sudden death), whereas 86 (45%) dogs (resistant to sudden death) survived. BRS was assessed by the phenylephrine method and was expressed by the regression line relating RR intervals to blood-pressure changes. BRS was significantly lower among susceptible than among resistant dogs (9.1 +/- 6.0 vs. 17.7 +/- 6.5 msec/mm Hg, p less than 0.0001). The risk for sudden death increased from 20% (15 of 73 dogs) for a BRS greater than 15 msec/mm Hg to 91% (62 of 68 dogs) for a BRS less than 9 msec/mm Hg (p less than 0.001). An internal control study in 55 animals showed that BRS was reduced 4 weeks after MI compared with control conditions (13.5 +/- 6.7 vs. 17.8 +/- 6.6 msec/mm Hg, p less than 0.001) and that a reduction occurred in 73% of animals. Susceptible dogs and those that spontaneously died after MI had a lower BRS even before the MI (16.2 +/- 5.9 vs. 22.2 +/- 6.2 msec/mm Hg, p less than 0.001). The risk for sudden death after MI increased from 35% (nine of 26 dogs) for a BRS before MI greater than 20 msec/mm Hg to 85% (17 of 20 dogs) for a BRS before MI less than 14 msec/mm Hg (p less than 0.001). This study demonstrates that the presence of a reduced BRS is associated with a greater susceptibility to ventricular fibrillation during subsequent ischemic episodes. In the majority of dogs, BRS is reduced after an MI. The results in 192 conscious dogs with a healed MI indicate that analysis of BRS is a powerful tool for risk stratification not only after, but even before, the occurrence of an MI.

Animals↗
PubMed1986

Mapping of body surface potentials in patients with the idiopathic long QT syndrome.

Body surface potential maps were recorded from 140 chest leads in 25 patients affected by the idiopathic long QT syndrome (LQTS) and in 25 healthy control subjects matched for age and sex. Potential time integrals of the QRST and ST-T intervals were calculated at each lead point and displayed as isointegral (ISOI) maps. The main abnormalities noted on the QRST and ST-T ISOI maps were one area of negative values larger than normal in the right anterior and inferior thorax and a complex multipeak distribution of the integral values. At least one abnormality was present in 19 (76%) of the patients with LQTS and four (16%) of the control subjects (p less than .001). Each ISOI map was also represented as a weighted sum of nine fundamental components (eigenvectors) to detect and quantitate the nondipolar content. The percent contribution of the nondipolar eigenvectors (all eigenvectors beyond the third) was significantly higher in the LQTS group than in the control group (p less than .005). Specifically, an abnormally high nondipolar content on the QRST ISOI maps was observed much more frequently for patients with LQTS than for control subjects (nine or 36% vs one or 4%), and this was also true on the ST-T ISOI maps (14 or 56% vs one or 4%). No correlation was found between the major abnormalities on body surface maps and syncopal episodes. However, the high prevalence (76%) of these alterations among the patients with LQTS and their infrequent occurrence in the control population strongly suggests that they may be useful markers for the diagnosis of atypical cases. The prominent electronegative area on the anterior thorax can be related to delayed repolarization of a portion of the anterior wall of the heart. This finding is in agreement with the hypothesis that lower than normal right cardiac sympathetic activity is the main pathogenetic mechanism of LQTS. Multipeak distribution and high nondipolar content suggest regional electrical disparities in the ventricular recovery process. This may in part account for the high susceptibility of patients with LQTS to malignant arrhythmias.

Adolescent↗
PubMed1985

Lack of correlation between occlusion and reperfusion arrhythmias in the cat.

Recently it has been stated that in dogs absence of arrhythmias during coronary artery occlusion identifies a subgroup at almost no risk for developing ventricular fibrillation (VF) during reperfusion. A potential implication would be that prevention of ischemic arrhythmias may also prevent the most severe reperfusion arrhythmias. This concept is at variance with available clinical evidence. In order to reexamine this problem the left anterior descending coronary artery was occluded for 20 minutes in 41 anesthetized cats; the incidence and type of arrhythmias during occlusion and during the first minute of reperfusion were analyzed. Five animals had VF during occlusion and were not resuscitated. Twenty animals had ischemic arrhythmias, and among them the incidence of reperfusion VF was 50%. Sixteen animals did not have ischemic arrhythmias, but they did have a very similar incidence of reperfusion VF (44%). Thus, in this feline preparation, absence of ischemic arrhythmias did not help to predict a favorable outcome at the moment of reperfusion. This disparity with previous studies does not depend on the protocol used, but it may be partly due to species difference. These results demonstrate a lack of correlation between reperfusion VF and ischemic arrhythmias and provide further support for the concept of different mechanisms involved in occlusion and reperfusion arrhythmias.

Animals↗
PubMed1983

[Citicoline activity in senile mental decay].

A brief report on the role of neurotransmittors (especially dopamine) depletion in cerebral aging and the development of certain pathological conditions in the elderly is presented. This is followed by a report on the results obtained by the administration of citicoline (500 mg/per diem intramuscularly for 20 days) to a group of 24 elderly patients with senile mental decay. A significant improvement (p less than 0.01) in mental performance was observed in all patients and no side effects were noted.

Aged↗