Lorenzo De Caprio

Hemodynamic effects of magnesium sulfate on the normal human heart

Abstract Because of its antiarrhythmic properties,1 parenteral magnesium sulfate has been widely used in the last decades in treating several supraventricular or ventricular arrhythmias2,3 even in patients with cardiovascular diseases. Recently, intravenous magnesium sulfate has proved effective in treating arrhythmias associated with acute myocardial infarction4 and long QT syndrome.5 However, a systematic evaluation of its effects on cardiovascular hemodynamics has not been reported. Recent experimental6 and clinical7 observations have suggested that magnesium sulfate may exert a vasodilator effect on human coronary arteries. The present study investigates the effects of magnesium sulfate infusion on coronary and systemic hemodynamics in humans.

Effects of histamine on coronary hemodynamics in humans: Role of H1and H2receptors

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)

QTQS2 ratio as an index of autonomic tone changes

The effects of changes in sympathetic tone on QT/QS2 ratio were studied in 10 healthy subjects aged 21 to 24 years. The subjects underwent a bicycle ergometer exercise, a tilt test, a decrease in carotid transmural pressure induced by means of pneumatic neck chamber, an i.v. injection of phenylephrine. A phonocardiogram and ECG were simultaneously recorded at a paper speed of 100 mm/s to evaluate QT and QS2 intervals in each test. In basal conditions, the QT/QS2 ratio was less than 1, whereas it increased progressively during the physical exercise and became greater than 1 at peak exercise. Both the upright position and the increase in neck-tissue pressure induced a significant increase in the QT/QS2 ratio as compared with the basal values, whereas i.v. administration of phenylephrine reduced significantly the QT/QS2 ratio. These results demonstrate that those stimuli which induce a rise in adrenergic activity may increase the QT/QS2 ratio. In contrast, the reflex inhibition of the adrenergic activity induced by phenylephrine is accompanied by a reduction in QT/QS2 ratio. Therefore, the QT/QS2 ratio might represent a reliable index of sympathetic cardiac tone.

R wave amplitude changes during stress testing. Comparison with ST segment depression and angiographic correlation

Abstract One-hundred and seven exercise stress tests and coronary angiograms were reviewed retrospectively, in order to evaluate the usefulness of R wave amplitude changes (ΔR) during exercise compared with ST segment depression in the screening of patients with coronary artery disease (CAD). We also attempted to correlate ΔR with the severity of CAD as expressed by coronary arteriography and left ventriculography. Thirty-six patients showed no coronary artery narrowing (0-V); the remaining 71 patients with stenosis of 70% of at least one of the major coronary arteries were divided into three groups. Sixteen patients had single vessel disease (1-V); five (31%) in this group showed abnormal left ventricular wall motion. Thirty-one patients had two-vessel disease (2-V); 22 (71%) of the 31 demonstrated abnormal left ventricular wall motion. Twenty-four patients had three-vessel disease (3-V); 20 (83%) of the 24 showed abnormal left ventricular wall motion. We considered ΔR values ≥ 0 and ST segment depression ≥ 1 mm. significant for diagnosis of CAD. The sensitivity of the ΔR method in predicting CAD was superior to the method based upon ST segment depression; however, the latter was significantly (P We found ΔR values ≥ 0 more frequently in the 2-V and 3-V groups as compared with the 1-V group. Patients of the 2-V and 3-V groups had a significantly higher incidence of abnormal left ventricular wall motion (P Even though the accuracy of the ΔR method was greater in more severe CAD, it seems to be offset by a concomitant decrease in specificity.

Influence of heart rate on exercise-induced R-wave amplitude changes in coronary patients and normal subjects

In order to study whether different heart rates achieved at peak exercise by normal subjects and patients with coronary artery disease (CAD) affect the results of analysis of R-wave amplitude changes (delta R), we evaluated delta R at progressively increasing heart rate (HR) steps in 60 normal subjects with negative exercise tests (ET), in 130 patients with CAD, in 88 patients with true positive and 42 with false negative ET, and in 43 patients with no CAD and false positive ET. We found that the sensitivity and specificity of delta R were HR dependent, the former decreasing and the latter increasing with progressively increasing HR steps. Mean values of delta R did not discriminate among the four groups for HRs up to 150 bpm; significant differences were found between normal subjects and CAD patients, both with true positive and false negative stress tests, at HR greater than 150 bpm. False positive patients had mean delta R similar to those found in normal subjects. We hypothesize that quantitative delta R analysis could be useful in ECG diagnosis of false negative and false positive patients at HR greater than 150 bpm.

Protective role of collaterals in patients with coronary artery occlusion.

We reviewed the clinical, hemodynamic and angiographic data of 105 patients with right coronary artery occlusion and 82 patients with left anterior descending coronary artery occlusion, subdivided into 3 groups by the presence and quality of collaterals to the occluded coronary (absent, poor or good collaterals). We found that patients with right coronary artery occlusion and good collaterals had a lower frequency of diaphragmatic myocardial infarction (60%) than patients with absent collaterals (100%) (P less than 0.01). In addition, in patients with old diaphragmatic myocardial infarction, both poor and good collaterals were associated with a lower frequency of severe asynergy of the diaphragmatic left ventricular segments at left ventriculography (54% and 14%, respectively), compared to patients with no collaterals to the right coronary artery (92%, P less than 0.02 vs. poor collaterals, P less than 0.001 vs. good collaterals). In contrast, in patients with left anterior descending coronary artery occlusion, the presence of either poor or good collaterals to the left anterior descending coronary artery was not associated with a lower frequency of old anterior myocardial infarction, or, in patients with old anterior myocardial infarction, with a less severe asynergy of the anterior left ventricular segments. Our results suggest that collaterals are effective in protecting the diaphragmatic left ventricular wall in patients with right coronary artery occlusion, but not the anterior left ventricular wall in patients with left anterior descending coronary artery occlusion.

Regional coronary hemodynamic effects of diltiazem in man

We evaluated the changes in regional coronary hemodynamics induced by diltiazem, 0.25 mg/kg intravenously, in nine patients with 75% to 90% diameter stenosis of the left anterior descending coronary artery (LAD) (group 1) and in 10 patients with 100% occlusion of the LAD and collaterals to the distal LAD (group 2). Although diltiazem induced similar changes in systemic hemodynamics in the two groups, a decrease in anterior coronary vascular resistance (ACVR) and an increase in great cardiac vein flow (GCVF) were observed after administration of diltiazem in all patients in group 1 but in only 6 of 10 patients in group 2 (subgroup 2B). ACVR increased and GCVF decreased after administration of diltiazem in 4 of 10 patients in group 2 (subgroup 2A). Clinico-angiographic characteristics, origin of collaterals, and diltiazem-induced changes in systemic hemodynamics were similar in subgroups 2A and 2B. Thus diltiazem increases coronary flow distal to a stenotic coronary artery but can decrease regional coronary flow and increase regional coronary resistance in a minority of patients with an occluded coronary artery supplied by collaterals, probably through a steal mechanism.

Relationship between ventricular ectopic beat frequency and heart rate: Study in patients with severe arrhythmias

To evaluate and quantify the relationship between premature ventricular contractions (PVCs) and heart rate (HR), 57 patients (48 men and 8 women, mean age 59.8 +/- 7.9 years) with severe PVCs (Lown-Wolf grade > or = 3a) over 24 hours of Holter monitoring were studied. Twenty had no coronary artery disease (CAD), 25 had angiographically documented CAD, and 12 had acute myocardial infarction. All parameters of the 24-hour recordings from two ECG leads were measured by a Holter analyzer designed in our laboratory, based on fast microprocessors and controlled by a microcomputer. Scatter diagrams of the number of PVCs per minute as a function of HR and correlation coefficient were computed for various HR values corresponding to a total number of minutes greater than five. A positive correlation (r > or = 0.35) was found in most patients without CAD (85%); there was a complex relationship between the strength of the correlation and the presence of CAD or acute myocardial infarction because of a greater variability in the results of correlation coefficient analysis (coefficient of variation 62%, 208%, and 145% in patients without CAD, with CAD, and with acute myocardial infarction, respectively). The incidence of a positive correlation was similar in patients with Lown-Wolf grade III (63%), IVa (82%), or > or = IVb (67%) arrhythmias. The reproducibility of the correlation coefficient of the relationship between PVC frequency and HR was tested in 15 patients. The mean value of the correlation coefficient was 0.801 +/- 0.169 for the first test and 0.805 +/- 0.22 (p = NS) for the second test.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of intracoronary gallopamil on coronary hemodynamics and myocardial oxygen consumption in humans

Summary: The response of coronary hemodynamics to the intracoronary (i.c.) bolus administration of gallopamil, 1.5 and 3.0 μg/kg, was evaluated in 14 patients with normal coronary arteries. Gallopamil, 3.0 μg/kg, induced a small and transient decrease in systolic and mean arterial pressure and a small increase in the preejection period. Coronary sinus blood flow increased significantly at 30 s (p < 0.01) and returned to baseline 10 min after gallopamil administration. Coronary vascular resistance was still reduced at 10 min and returned to baseline at 15 min. Myocardial O2 consumption and extraction decreased significantly (p < 0.01) at 30 s. While myocardial O2 consumption returned to baseline 15 min after gallopamil administration, myocardial O2 extraction was still significantly reduced at this time. Milder and more transient changes were observed after i.c. administration of the lower dose (1.5 μg/kg), and no significant changes were found after i.c. administration of saline. These data show that i.e. gallopamil, in patients with normal coronary arteries, induces direct, transient, and dose-related peripheral coronary vasodilation. The reduction of myocardial O2 consumption and extraction suggests a direct negative inotropic and metabolic effect of gallopamil.

Direct coronary vasodilator effects of intracoronary histamine administration in humans

Summary: Histamine is widely present in human tissues and can be released by immunologic and nonimmunologic reactions. Although several direct cardiovascular effects of histamine have been demonstrated in humans, little is known about the direct effects of histamine on the human coronary circulation in vivo. Therefore, we investigated the changes in coronary hemodynamics induced by bolus intracoronary administration of 4 μg of histamine to 11 patients with angiographically normal coronary arteries under continuous monitoring of R-R interval from the electrocardiogram, arterial pressure (AP), and coronary sinus blood flow (CBF), measured by thermodilution. Immediately after the end of the intracoronary histamine bolus, with R-R interval and AP unchanged CBF increased from 144 ± 20 to 238 ± 27 ml/min (p < 0.01) and coronary vascular resistance decreased from 0.7 ± 0.16 to 0.42 ± 0.1 mm Hg/ml/min (p < 0.01). No change in coronary hemodynamics was observed after bolus intracoronary administration of physiologic saline. The effects of histamine on systemic hemodynamics consisted of a transient fall in AP and in R-R interval, starting after the onset of changes in coronary hemodynamics. These data show that histamine possesses a direct coronary vasodilator effect in humans, independent of the determinants of myocardial oxygen consumption.