Incremental biorate control ventricular pacing and ventricular arrhythmogenicity.
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Arrhythmias, Cardiac↗
Biomedical subjects
M Condorelli
Publications and source records attributed to M Condorelli.
Reversal of left ventricular hypertrophy following treatment with beta-blockers: experience with tertatolol.
Hypertrophy in response to increasing blood pressure in primary hypertension leads to important functional consequences for the left ventricle. In fact, the progression of hypertensive heart disease, from an adaptive left ventricular hypertrophy with compensated ventricular function to severe hypertrophy with left ventricular failure, has been long thought to be related to the severity and duration of hypertension. Antihypertensive treatment seems to prevent or minimize the occurrence of left ventricular hypertrophy, but questions arise as to whether this therapy is also able to restore normal hemodynamic conditions, or at least to minimize the hemodynamic abnormalities. This review aims at summarizing current knowledge on the effects of the antihypertensive treatment with beta-blockers, including tertatolol, on hypertension-induced left ventricular hypertrophy. The pathogenetic mechanisms underlying the cardiovascular changes associated with hypertension are discussed. A decrease in left ventricular wall thickness as well as in left ventricular mass has been reported in most of the studies performed with different types of beta-adrenergic blocking agents. The extent of this reduction seems to be related not only to the fall in systemic blood pressure, but also to a decrease in sympathetic stimulation. With regard to the functional consequences of hypertension, the reversal of left ventricular hypertrophy following antihypertensive treatment with beta-blockers is usually associated with an improvement in left ventricular performance. This phenomenon can hardly be ascribed to the direct effects of beta-blocking agents. It is more likely to be related to the concomitant reduction in the afterload and to the improved left ventricular compliance, associated with a decrease in left ventricular wall thickness.
Adrenergic beta-Antagonists↗
Impaired responsiveness of the ventricular sensory receptor in hypertensive patients with left ventricular hypertrophy.
We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = -29.9, for patients with hypertension = -40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by -40 mm Hg LBNP in normal subjects (+107 +/- 5 vs +129 +/- 15 mm Hg/ml/sec, p less than .05) but not in patients with hypertension. Consequently, the slope of the delta CVP/delta FVR regression was reduced in normal subjects (-20.6, p less than .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of -10 and -40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to -40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.
Adult↗
Relation between QT and QS2 intervals during exercise and recovery. Response in patient with coronary artery disease and age-matched control subjects.
We investigated the relationship between QT interval and QS2 (electromechanical systole) during exercise and recovery in patients with coronary artery disease (CAD) and exercise-induced myocardial ischemia (n = 12), and in age-matched controls (n = 20). Upright bicycle exercise was performed (50 watts/min + 20 watts/min every 2 min), recording electrocardiographic lead 2 (100 mm/sec) for QT and QS2 measurement at rest, at each step of uninterrupted exercise and every 60 sec during a 3-min recovery period. Resting data showed a QT less than QS2 finding in both groups; during exercise, QT and QS2 decreased. The values of QT and QS2, collected at each step of exercise and plotted against heart rate (HR) separately for both groups, showed a significant correlation coefficient. Comparing the regression lines of HR-QT and HR-QS2 separately for both groups, we found that both intervals decreased in parallel and the mean QT remained shorter than QS2 in both groups during exercise. The QT/QS2 ratio remained unchanged significantly during exercise and recovery in CAD. In control subjects, the ratio remained unchanged during exercise and the first min of recovery, while a significant change was detected in late (2,3 min) recovery from an adrenergic-induced effect. The mean exercise-induced response of QT-QS2 relationship includes a QT less than QS2 pattern in both groups. In CAD patients, an abnormal pattern was found in two patients during recovery by a relative prolongation of QT, suggesting the possibility of a risk factor for dangerous arrhythmias or sudden death.
Blood Pressure↗
Effects of prostaglandin synthesis inhibition on sympathetic-and parasympathetic-mediated coronary hemodynamic responses.
In chloralose-anesthetized dogs with the left circumflex coronary artery perfused at constant flow, the effects of indomethacin or naproxen on coronary and systemic responses to sympathetic and parasympathetic stimulation were evaluated. Sympathetic stimulation was evoked either by 1-min carotid artery occlusion or by epinephrine (5 micrograms) or norepinephrine (5 micrograms) intracoronary administration. Reflex or direct parasympathetic stimulation was produced by ouabain (40 micrograms) or acetylcholine (2.5 micrograms) injection, respectively, in the perfused coronary artery. The administration of indomethacin or naproxen reduced the integrated areas of coronary vasodilatation induced by epinephrine and norepinephrine. The extent of this reduction was dose-dependent with both indomethacin (epinephrine: r = 0.774, n = 35, P less than .001; norepinephrine: r = 0.766, n = 35, P less than .001; norepinephrine: r = 0.799, n = 35, P less than .001) up to 1.5 and 7 mg/kg, respectively. Further increase in dosage of both prostaglandin synthesis inhibitors failed to induce further reduction of integrated areas of coronary vasodilatation. In contrast, the maximum fall in coronary perfusion pressure, induced by both catecholamines, remained unmodified after inhibition of prostaglandin synthesis, whereas a faster return of the perfusion pressure to base line was observed. The extent of cyclooxygenase activity inhibition induced by indomethacin or naproxen, assessed through the radioimmunoassay of thromboxane B2, showed a consistent dose-dependent increase until complete inhibition was attained with 1.5 mg/kg of indomethacin and 7 mg/kg of naproxen. No significant change in the coronary and systemic hemodynamic response induced by carotid occlusion and by ouabain or acetylcholine intracoronary administration was observed. Furthermore, complete cyclooxygenase inhibition, induced by either indomethacin or naproxen, was able to reduce the coronary vasodilatation induced by isoproterenol (5 micrograms) intracoronary injection but failed to modify the coronary vasoconstriction elicited by both epinephrine and norepinephrine in propranolol-treated dogs. These data indicate that the prostaglandin system is involved in the coronary vasodilatation induced by humoral sympathetic stimulation, whereas coronary hemodynamic responses to both neural sympathetic or parasympathetic stimulation are not influenced by the administration of prostaglandin synthesis inhibitors.
Acetylcholine↗
Noninvasive techniques in clinical pharmacology. Time intervals in assessment of vasodilators in coronary artery disease.
We enrolled 15 male volunteers with angiographic evidence of coronary artery disease (CAD) to investigate the effects of sublingual administration, on different days, at random, of placebo and three drugs with different action such as isosorbide dinitrate, nifedipine and molsidomine. We recorded simultaneously electrocardiogram, phonocardiogram and carotid pulse at paper speed of 100 mm/s; blood pressure was measured by auscultatory method. We calculated the systolic time intervals (STI) being noninvasive indices of left ventricular function and the ratio of diastolic time to heart rate (%D), well related to coronary blood flow in patients with severe obstructive lesions. Placebo decreased heart rate (HR) without effects on STI or %D. Isosorbide dinitrate induced a prolonged pre-ejection period (PEP) (by decreasing preload), tachycardia and a significantly decreased %D, suggesting a fall in coronary blood flow time. Nifedipine decreased diastolic blood pressure and values of PEP (by decreasing afterload) without effects on %D. Finally, molsidomine prolonged PEP (by decreasing preload) without reflex induced tachycardia and changes of %D. In conclusion, mechanocardiography can be useful in noninvasive assessment of vasodilators in CAD patients.
Blood Pressure↗
[Incidence and complexity of ventricular arrhythmias in dilated cardiomyopathy. Evaluation by dynamic ECG. Preliminary report].
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Adolescent↗
Iatrogenic occlusion of the left anterior descending coronary artery. A case report.
A 27-year-old man with mixed aortic stenosis and regurgitation formerly stabbed in the left anterior part of the chest was admitted to our department with dyspnea. Coronary arteriography, performed during cardiac catheterization, showed total occlusion of the left anterior descending coronary artery. The Authors point out the iatrogenic cause of the coronary occlusion. It was due to ligation of the artery when suturing the ventricular wound.
Adult↗
Transvenous catheter ablation of the accessory atrioventricular pathway in the permanent form of junctional reciprocating tachycardia.
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Adult↗
Evidence for an adenosine A2/Ra receptor on human basophils.
5'-N-ethylcarboxamideadenosine (NECA) greater than 2-chloroadenosine greater than adenosine greater than (-)-N6-(R-phenyl-isopropyl)-adenosine greater than (+)-N6-(S-phenylisopropyl)-adenosine, in that order of potency, inhibited in vitro antigen-induced histamine release from human basophils in a dose-dependent fashion. Inhibition occurred only during the first stage of antigen-induced histamine release and the nucleosides failed to inhibit the release caused by the Ca2+ ionophore, A23187. 6-nitrobenzylthioinosine and dipyridamole, which inhibit adenosine uptake, and erythro-9-(2-hydroxy-3-nonyl)adenine, which blocks adenosine metabolism, did not impair the inhibition caused by NECA and adenosine. 8-phenyltheophylline and theophylline, two competitive antagonists of adenosine receptors, blocked the inhibition caused by NECA and adenosine. These data suggest that NECA and other adenosine analogs activate a specific cell surface adenosine receptor which possesses properties similar to those of an adenosine A2/Ra receptor.
Adenosine↗
Role of prostaglandins in the renal handling of a salt load in essential hypertension.
Renal function and systemic hemodynamics were assessed in 10 hypertensive patients and in 10 age-matched normotensive subjects during control conditions (80 mEq of sodium/day) and after a salt load, either alone (480 mEq/day) or combined with indomethacin or sulindac. Indomethacin was used to induce ubiquitous inhibition of prostaglandin synthesis and sulindac to inhibit prostaglandin synthesis in all tissues except the kidney. Under control conditions there was no significant difference between the 2 groups in any measurement except blood pressure and total peripheral resistance. Also, the changes induced by salt load in the 2 groups were comparable. However, after indomethacin administration, only hypertensive patients showed a significant reduction in the 24-hour sodium excretion (from 417 +/- 61 to 317 +/- 49 mEq, p less than 0.05), so that the difference between this value and the corresponding value of normotensive subjects (453 +/- 79 mEq) became significant (p less than 0.05). The changes in sodium excretion in hypertensive patients were significantly correlated with the changes in renal plasma flow (r = 0.803, p less than 0.01). However, cardiac output and renal blood flow showed a similar pattern in normal and hypertensive persons. Finally, after the addition of sulindac to salt load, the differences in the 24-hour sodium excretion vanished. These results were also confirmed in an ancillary study performed, using the same protocol, in 10 other hypertensive patients using ibuprofen rather than indomethacin. Our data suggest that renal prostaglandins participate in renal disposal of chronic salt load in hypertensive patients but not in normal persons.
Adolescent↗
24-hour blood pressure recording in patients with orthostatic hypotension.
Continuous intra-arterial blood pressure measurement and electrocardiograms were obtained in two ambulatory patients with orthostatic hypotension due to autonomic dysfunction. Systolic and diastolic arterial pressure presented marked variations which took place mainly during the day and were related to several physical activities; however, marked falls in blood pressure were also observed during sleep and at the moment of arousal. A peak incidence of hypotensive events was found in the afternoon, mainly in the hours following the afternoon meal. Recording was repeated after 3 weeks of treatment with propranolol, 40 mg t.i.d. In patient 1, beta blockade drastically reduced the number and severity of hypotensive episodes, while propranolol failed to control blood pressure in patient 2, who experienced a higher number of hypotensive events during treatment. Findings of this study may be relevant to the management of patients with orthostatic hypotension and should contribute to a more accurate characterization of blood pressure profile in autonomic dysfunction.
Blood Pressure↗
Histamine release from human basophils by pepstatin A.
Pepstatin A, a pentapeptide isolated from cultures of actinomycetes, induced histamine secretion from human basophils in the concentration range of 3 X 10(-7) to 10(-4) M. The characteristics of this reaction were similar to those of f-met-peptide-induced histamine release: pepstatin A-induced release required Ca2+ and the release reaction was complete within 2 min at 22 or 37 degrees C, but did not occur at 4 degrees C. Release by both pepstatin A and f-met-peptide was reversibly inhibited by two non-releasing analogs of f-met-peptide, CBZ-Phe-Met and BOC-Met-Leu-Phe. Further, there was complete cross-desensitization between pepstatin A and f-met-peptide, while cells desensitized to pepstatin A released normally with anti-IgE and vice versa. A variety of pharmacological agents had similar effects on both pepstatin A and f-met-peptide-induced release (e.g., no enhancement with D2O; marked enhancement with cytochalasin B). We suggest that pepstatin A induces histamine release from human basophils by activating a cell surface receptor(s), also activated by the synthetic tripeptide f-met-peptide.
Basophils↗
Asymptomatic transient ST changes during ambulatory ECG monitoring in diabetic patients.
The reported higher incidence of painless myocardial infarction in diabetic patients suggests that asymptomatic transient myocardial ischemia may also be frequent in diabetes. To explore this possibility 51 subjects with type II diabetes, aged 43 to 71 years (mean +/- SEM 56 +/- 8), 70 nondiabetic patients with coronary artery disease (mean age 55 +/- 5), and 40 nondiabetic patients without overt coronary disease (age 54 +/- 9) were studied. Thirty-eight of the 51 diabetic patients (74%) had evidence of associated coronary disease and 19 (37%) had evidence of previous myocardial infarction. All subjects underwent continuous 24-hour ambulatory ECG monitoring. In 18 of 51 diabetic patients 93 episodes (73% of the total number) of asymptomatic ST segment changes were recorded; the total number of symptomatic episodes was 36, and they were observed in seven patients (27%). Forty-eight (60%) asymptomatic and 32 symptomatic episodes of significant ST changes were found in nondiabetic patients with coronary artery disease. When patients with previous myocardial infarction were examined separately, asymptomatic episodes of significant ST changes were observed in 10 of 19 diabetic patients and in 5 of 25 nondiabetic patients with coronary artery disease (p less than 0.05). In an additional 28 diabetic patients who underwent exercise stress test, 15 exhibited an abnormal ECG response; however, only five of them (33%) were symptomatic. This study suggests that the incidence of transitory myocardial ischemia, as assessed by ambulatory ECG monitoring and exercise stress test, is higher in type II diabetic patients than in nondiabetic control subjects with coronary artery disease.
Adult↗
Carotid sinus reflex control of coronary blood flow in human subjects.
Systemic and coronary hemodynamics were assessed before and during a reduction in carotid transmural pressure. This reduction was induced by means of a pneumatic neck chamber in 15 normal subjects and 15 hypertensive patients with a normal coronary arteriogram. A reduced baroreflex responsiveness was demonstrated in hypertensive patients as compared with normal subjects by evaluating both the reflex bradycardia evoked by intravenous administration of phenylephrine and the reflex increase in blood pressure during carotid sinus hypotension. In normal subjects, the reduction in carotid transmural pressure induced a significant increase in mean blood pressure, total peripheral resistance, cardiac output, heart rate, coronary vascular resistance, coronary blood flow assessed by the continuous thermodilution method and myocardial oxygen consumption. In hypertensive patients, the same stimulus significantly increased mean blood pressure, cardiac output, heart rate and coronary blood flow while no significant change was detected in coronary vascular resistance and myocardial oxygen consumption. The increase in mean blood pressure, total peripheral resistance and cardiac output was significantly higher in normal subjects than in hypertensive patients. These results suggest that in normal subjects carotid sinus hypotension evokes reflex coronary vasoconstriction, whereas this response is blunted in hypertensive patients with reduced baroreflex sensitivity.
Adult↗
Chronic amiodarone therapy and hypokalemia.
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Amiodarone↗
Late phase of nitroglycerin-induced coronary vasodilatation blunted by inhibition of prostaglandin synthesis.
In chloralose-anesthetized dogs with the left circumflex coronary artery perfused at constant flow, the effects of increasing doses of indomethacin or naproxen on the coronary and systemic hemodynamic responses to a 5 microgram intracoronary injection of nitroglycerin (NTG) were evaluated. The integrated areas of NTG-induced coronary vasodilatation were reduced after administration of indomethacin or naproxen. The extent of this reduction was increased progressively by augmenting the dose of indomethacin and naproxen up to 1.5 and 7 mg/kg, respectively. We also assessed the extent of cyclooxygenase inhibition induced by indomethacin or naproxen through the radioimmunoassay of thromboxane B2, which reflects thrombin-induced activation of platelet thromboxane A2 production during whole blood clotting. The level of inhibition progressively increased and complete inhibition was attained with 1.5 mg/kg indomethacin and 7 mg/kg naproxen. Further increase in dosage failed to induce further reduction of integrated areas of coronary vasodilatation, and a correlation was found between the extent of the reduction of the integrated areas of coronary vasodilatation and the dose of indomethacin (r = .828, n = 35, p less than .001) or naproxen (r = .729, n = 35, p less than .001). Finally, the NTG-induced maximum fall in coronary perfusion pressure remained unmodified after inhibition of prostaglandin synthesis, but there was a faster return of the perfusion pressure to the basal value.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Participation of endogenous catecholamines in the regulation of left ventricular mass in progeny of hypertensive parents.
To investigate whether adrenergic activity is a determinant of left ventricular hypertrophy in human hypertension, in each of 10 normotensive subjects with two hypertensive parents we have examined the relationship between changes in echocardiographic parameters of left ventricular anatomy and those in circulating catecholamine levels induced by three, 3 week periods of different sodium and potassium intakes. A high sodium-normal potassium regimen induced a significant reduction in upright plasma norepinephrine (from 599 +/- 89 to 379 +/- 45 pg/ml, p less than .01) and in posterior wall (PWT) and interventricular septal (IVST) thickness, as well as in the left ventricular mass index (LVMi). Changes in upright plasma norepinephrine concentrations correlated with those in IVST (r = .822, p less than .01) and in LVMi (r = .833, p less than .01). A low sodium-normal potassium diet resulted in increases in supine and upright plasma norepinephrine levels (from 356 +/- 44 to 488 +/- 89 pg/ml, p less than .001; and from 565 +/- 42 to 744 +/- 33 pg/ml, p less than .01) as well as increases in IVST and LVMi (from 97 +/- 7 to 107 +/- 7 g/m2, p less than .001). The changes in norepinephrine levels in supine and upright subjects correlated with changes in IVST (r = .836, p less than .01 and r = .796, p less than .01) and in LVMi (r = .931, p less than .001 and r = .947, p less than .001). No significant change in plasma catecholamine concentrations or in PWT, IVST, or LVMi was detected after a low sodium-high potassium regimen.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗