Reperfusion ventricular arrhythmias in a 75-year-old subject with Prinzmetal's angina.
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Biomedical subjects
Publications and source records attributed to F Rengo.
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The toxic effect of calcium overload and the action of magnesium sulfate (4 mM) and magnesium chloride (4 mM) on heart rate, coronary flow rate, left ventricular systolic pressure, dp/dt max and voltage epicardial electrogram were studied in the isolated and perfused rat heart. Increasing calcium load by increasing [Ca]o from 1 to 6 mM we observed a progressive increase in heart rate coronary flow rate, left ventricular systolic pressure, dp/dt max and a decrease in voltage epicardial electrogram. During the exposure to [Ca]o 8 mM the toxic manifestations of calcium overload developed and we observed a reduction in heart rate, coronary flow rate, left ventricular systolic pressure, dp/dt max and an increase in voltage epicardial electrogram. Magnesium sulfate and magnesium chloride had similar effect: in fact, in both procedures we observed a decrease in heart rate, left ventricular systolic pressure, dp/dt max, voltage epicardial electrogram and an increase in coronary flow rate at [Ca]o 2 mM. When magnesium salts were administered at the same time as the heart was exposed to [Ca]o 8 mM, we observed a reduction in the toxic effect of calcium overload. When magnesium salts were administered after the appearance of the calcium overload, they did not revert the toxic effect of calcium overload but prevented the insurgence of cardiac standstill. Thus, in the isolated perfused rat heart, the toxic manifestations of calcium overload develop at [Ca]o 8 mM and magnesium salts are able to reduce the toxic effects of calcium overload and the appearance of cardiac standstill according to their calcium-antagonism mechanism.
The relationship between QT/QS2 ratio and angiographic severity of coronary heart disease (CHD) was determined in 99 patients who underwent coronary arteriography because of chest pain. Sixteen control patients with normal coronary arteriograms and normal left ventricular function and 83 patients with angiographic evidence of CHD were studied. QT/QS2 ratio and systolic time intervals were calculated from poligraphic recordings taken at rest. In control subjects QT/QS2 ratio was significantly shorter (0.91 +/- 0.04) than in patients with double (0.95 +/- 0.07; p less than 0.05 versus control subjects) and triple vessel coronary artery disease (0.95 +/- 0.05; p less than 0.05 versus control subjects). QT/QS2 ratio was significantly higher (p less than 0.01) in patients with 3 areas or more of left ventricular abnormal wall motion (LV AWM) (0.98 +/- 0.05) than in patients with none (0.92 +/- 0.06) or just 1-2 areas (0.93 +/- 0.06) of LV AWM. Multiple regression analysis revealed no relation between the number of coronary stenoses and QT/QS2 (t = 0.86; p = NS), while a relation was identified between the number of asynergic segments and QT/QS2 (t = 1.99; p less than 0.05). A significant correlation was found between QT/QS2 and PEP/LVET (r = 0.39; p less than 0.001). Setting the upper normal limit at 2 standard deviations from the mean of control subjects (QT/QS2 = 0.99), QT/QS2 criterion yielded a 30% sensitivity, a 94% specificity and a 96% predictive accuracy in diagnosing CHD. We conclude that in CHD patients QT/QS2 ratio is influenced by the extension of LV AWM. Although a low sensitivity may limit its use, a QT/QS2 value higher than 0.99 in a patient with chest pain strongly suggests CHD and thus this criterion may be diagnostically useful.
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To evaluate whether histamine exerts a direct effect on coronary hemodynamics in humans, and to investigate the role played by H1 and H2 receptors in this response, intracoronary saline solution or histamine (4 micrograms) was administered in 10 patients with normal coronary arteries during diagnostic cardiac catheterization. Histamine injection was repeated after intravenous cimetidine (400 mg) and diphenhydramine (10 mg). The electrocardiogram, arterial pressure and thermodilution coronary blood flow were continuously monitored during and for 40 seconds after each injection. Immediately after histamine injection there was a significant increase in coronary blood flow (65 +/- 6%) and a decrease in coronary vascular resistance (-40 +/- 3%) (both p less than 0.001), with minor changes in the RR interval and the mean arterial pressure. H2 receptor blockade with cimetidine did not affect these changes, while H1 receptor blockade with diphenhydramine significantly reduced the histamine-induced increase in coronary blood flow and the decrease in coronary vascular resistance (26 +/- 6%, p less than 0.005 and -18 +/- 5%, p less than 0.001, respectively). Twenty to 30 seconds after histamine injection, a significant decrease in mean arterial pressure (-17 +/- 2%, p less than 0.001) and in the RR interval (-4 +/- 1%, p less than 0.01) was observed. These changes persisted after H2 receptor blockade with cimetidine, but were completely abolished after H1 receptor blockade with diphenhydramine. In each case coronary and systemic hemodynamics returned to normal within 40 seconds of the injection.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of increased cholinergic activity on reperfusion induced ventricular arrhythmias was studied in alpha chloralose anaesthetised dogs by administering neostigmine during a 25 min occlusion of the anterior left descending coronary artery. The dogs were divided into five groups, each of 10 animals: the control group received only saline solution; group 1 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion (that is, 5 min before reperfusion); group 2 atropine 0.4 mg.kg-1 iv at 10 min of coronary occlusion and neostigmine 0.03 mg.kg-1 iv at 20 min; and group 3 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion and at the same time underwent atrial pacing at the same rate as that of the sinus node just before neostigmine administration. In group 4 heart rate was slowed (junctional rhythm) by destroying the sinus node at 20 min of coronary occlusion. The results obtained showed that ventricular tachycardia and fibrillation, which occur at the beginning of reperfusion, were significantly less frequent in group 1 (p less than 0.001) and in group 4 (p less than 0.001). The protective action of neostigmine was abolished by previous administration of atropine (group 2) and modified by preventing the decrease in the heart rate by atrial pacing (group 3). In group 3 ventricular tachycardia was more frequent but the incidence of ventricular fibrillation was reduced significantly compared with the control and atropine groups. Thus cholinergic activity has a protective role in reperfusion arrhythmias by decreasing the heart rate before release of the coronary occlusion and therefore reduces the incidence of ventricular fibrillation.
The authors describe a case of spontaneous angina during catheterization in a patient with left anterior descending and circumflex stenosis promptly relieved by diltiazem, 10 mg, given in the left ventricle. Coronary and systemic haemodynamics measured during and at the end of angina demonstrated an increase in blood flow to the ischaemic myocardium as the mechanism responsible for the diltiazem-induced angina relief.
In order to evaluate the diagnostic value of exercise-induced Q wave changes and its relationship with the extent of coronary involvement and presence and location of a previous myocardial infarction, we examined the stress electrocardiograms of 188 consecutive patients with chest pain. Coronary arteriography shoved single vessel disease (SV) in 28 patients and multivessel disease (MV) in 130 patients; a previous myocardial infarction was present in 64 patients. The Q wave amplitude was measured as average of ten values in CM5 at rest and at peak exercise; a Delta-Q less than 0, i.e. reduction or no change of Q wave at peak exercise, was considered a positive response for coronary artery disease. The Delta-Q criterion shoved a significantly better sensitivity than ST depression, as a whole, but this improvement was nullified when patients with anterior myocardial infarction were excluded; as well specificity of Delta-Q although better than ST, did not allow a significant improvement for the diagnostic value of stress test. We also evaluated the diagnostic accuracy for multivessel coronary artery disease of both criteria positive was 78% whereas the negative predictive value of both criteria negative was 91%. We concluded that the exercise-induced Delta-Q less than 0 is a good indicator of coronary artery disease, although not superior to ST depression; the negativity of both criteria seems to be highly reliable for the exclusion of multivessel coronary artery disease.
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Nifedipine, diltiazem and verapamil are three effective calcium-antagonists in the treatment of angina pectoris. We compared their effects on effort angina to evaluate whether one of them is more efficacious. The data were collected from 42 patients (37 males, 5 females; mean age 51 +/- 4) entering one of 3 different trials; the beginning of all trials comprised a two-week, single blind, placebo run-in phase. An exercise stress test was performed at the end of this period and it was considered as basal test for the statistical analysis. Then the 42 patients were divided in 3 groups of 14 and entered a double-blind, randomized phase of drug treatment. The 3 groups started 3 parallel trials: 1) placebo/nifedipine 60 mg/day; 2) placebo/verapamil 360 mg/day; 3) placebo/diltiazem 240 mg/day. The duration of each trial was of 6 weeks (3 weeks of treatment with placebo and 3 weeks with active substance). Exercise stress tests were performed at the end of each phase of the trials, and the resulting data were compared with the data of the test performed at the end of run-in period. Parameters evaluated were: heart rate, blood pressure and rate pressure product at basal conditions, at submaximal and peak exercise; moreover we considered workload, maximal ST segment depression, total exercise duration and frequency of exercise-induced angina. Verapamil reduced rate pressure product at basal condition; all three drugs reduced rate pressure product at submaximal exercise, but a significant statistical difference was found only for verapamil and diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)
Two-dimensional echocardiographic (2-D echo) and electrocardiographic (ECG) monitoring was performed in 53 patients with anginal chest pain during infusion of physiologic doses of epinephrine. Technically adequate 2-D echo studies were recorded in 45 patients. Of these 45 patients, 35 had significant coronary artery disease. Twenty-two patients showed ECG changes during the test (ECG sensitivity 63%), 13 of whom also showed wall motion abnormalities (2-D echo sensitivity 48.5%). Combined ECG and 2-D echo criteria of a positive test yielded a sensitivity of 74%. None of the 10 patients without coronary artery disease had electrical or mechanical abnormalities during the test (specificity 100%). Thus, the epinephrine test during simultaneous 2-D echo and ECG monitoring is a valid alternative to echocardiographic exercise stress testing. Furthermore, the adequate images obtained during the infusion allow better investigation of relation between wall motion abnormalities and ECG changes during myocardial ischemia.
Myocardial asynergies detected by two-dimensional echocardiography during intravenous administration of Dipyridamole (0.75 mg/kg) were evaluated in 54 patients referred for angiographic evaluation of chest pain. Technically adequate two-dimensional echocardiograms suitable for analysis were recorded in 42 of 54 (77.7%) patients studied. Thallium-201 myocardial perfusion scintigraphy, during dipyridamole test was performed in the same patients. Thirty of the 42 patients studied showed significant coronary narrowing at cardiac catheterization. Dipyridamole-induced wall motion abnormalities and myocardial perfusion defects were detected, respectively, in 19 (63.3%) and 21 (70%) of 30 patients with significant coronary artery disease. Wall by wall comparison of the distribution of dipyridamole-induced echocardiographic asynergy with reversible thallium-201 (201Tl) perfusion defects demonstrated complete correlation in 42 segments examined. Three segments with perfusion defects at thallium scanning did not show asynergy during the test while two segments showing wall motion abnormalities during dipyridamole infusion did not manifest perfusion defects. Our study demonstrates that two-dimensional echocardiography during dipyridamole testing is useful in detecting patients with coronary artery disease. Furthermore, ventricular asynergies detected during the test show a high correspondence with site of myocardial perfusion defects at thallium scanning.
In order to evaluate the clinical implications of QT/QS2 ratio during manoeuvres of sympathetic stimulation we studied the effects of handgrip (75% of maximal voluntary contraction) in 18 middle-aged normal subjects and in 16 patients with previous myocardial infarction. We also evaluated the effects of propranolol (0.1 mg/kg i.v.) in all normal subjects and in 10 of the 16 patients with coronary artery disease. At rest the two groups had similar heart rate, blood pressure, QT, QS2 and QT/QS2 ratio values. A significant increase in heart rate and systolic blood pressure was recorded during handgrip both in normal subjects and in patients with coronary artery disease; QT/QS2 significantly increased in normal subjects but did not show significant variations in patients with coronary artery disease, with significant differences between the two groups at peak exercise. Handgrip-induced QT/QS2 changes showed a marked variability both in normal and diseased subjects. After propranolol, QT/QS2 showed no significant difference at peak exercise in the two groups. The variability of ratio changes was nullified by the administration of the drug. These findings suggest that handgrip-induced QT/QS2 changes might be an expression of beta-adrenergic discharge. The clinical value of handgrip-induced QT/QS2 changes in detecting patients with coronary artery disease is limited by the variability of the response of the ratio observed in the two groups.