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By means of the Doppler ultrasonic flowmeter catheter, phasic instantaneous left ventricular blood velocity was measured at the mitral valves of 184 conscious human subjects during atrial arrhythmias. Atrial extrasystoles and pacemaker-induced atrial tachycardias reduced peak mitral valve blood velocities in direct relation to shortened diastolic cycle length. Atrial fibrillation with irregular ventricular responses produced beat-to-beat alternations of peak mitral velocity, with smaller peak mitral blood velocities usually associated with shortened R-R intervals on the electrocardiogram. This report represents the first comprehensive description of instantaneous and continous phasic blood velocity at the mitral valve during atrial arrhythmias in man. It is concluded that atrial tachyarrhythmias exert an adverse influence on left ventricular filling velocities.
J Thorac Cardiovasc Surg 1975 Feb
PMID:Blood velocity at mitral valve during atrial arrhythmias in man. 4 33

A placebo-controlled, double-blind crossover study was undertaken in 10 normal subjects to examine the effects of arotinolol (10 mg bid), a nonselective beta blocker with alpha-blocking activity, on exercise capacity and hormone levels during exercise after a 2-week treatment period. Maximal oxygen uptake (VO2 max) and blood lactic acid concentration (LA) were measured during progressive exercise testing. An exercise intensity equivalent to 4 mmol/l of LA was used for the constant workload exercise test. Humoral factors were measured after 20 minutes of constant workload exercise. The administration of arotinolol significantly decreased systolic blood pressure and heart rate at rest and during exercise, but diastolic blood pressure did not change. No significant difference was found between arotinolol and placebo with regard to VO2 max and maximal workload. Plasma renin activity (PRA), aldosterone (PAC), and norepinephrine (NE) levels at rest and during exercise did not differ between the two treatments. In contrast, plasma epinephrine (EN) levels at rest and during exercise were significantly greater with arotinolol. Atrial natriuretic peptide (ANP) at rest did not differ between the two treatments. However, exercise caused a significant increase in ANP after arotinolol treatment. These findings suggest that arotinolol decreases blood pressure and heart rate without affecting exercise capacity.
Cardiovasc Drugs Ther 1992 Aug
PMID:Effects of arotinolol on exercise capacity and humoral factors during exercise in normal subjects. 138 11

Atrial premature beats seldom require an antiarrhythmic treatment; reassurance and suppression of coffee, alcohol, and tobacco generally suffice. Acute atrial fibrillation is best treated by electrical cardioversion if it induces acute cardiovascular decompensation. If it is not poorly tolerated, the arrhythmia may be treated with digitalis at doses sufficient to keep the ventricular response rate at 70-90/min. This therapy may restore sinus rhythm, but conversion to sinus rhythm often requires the combined use of digitalis with a beta-blocker or class I antiarrhythmic drug (quinidine, disopyramide, procainamide, propafenone, or flecainide). Digitalis must be avoided in the presence of a preexcitation, and class IA agents, which facilitate atrioventricular (AV) nodal transport, must never be used without digitalis. Chemical cardioversion may also be achieved by i.v. amiodarone. Long-term prevention of recurrences after cardioversion or in the presence of recurrent paroxysmal atrial fibrillation requires digitalis combined with a class I agent, or a beta-blocker, preferably sotalol. Amiodarone is also very efficacious. Special mention should be made of atrial fibrillations of vagal or sympathetic origin, which are best treated by amiodarone, or beta-blockade (nadolol), respectively. In the presence of chronic established atrial fibrillation, digitalis in combination with a beta-blocking agent or a calcium antagonist, such as verapamil or diltiazem, may be useful to slow the ventricular response rate. If successful control cannot be obtained, catheter ablation of the AV node with implantation of a rate-responsive pacemaker must be contemplated. The therapeutic approach in patients with chronic atrial fibrillation, whether or not associated, is similar to atrial flutter.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1991
PMID:Antiarrhythmic treatment of atrial arrhythmias. 172 15

The effect of xipamide on plasma alpha-atrial natriuretic peptide and the renin-aldosterone-kallikrein system have been studied in 12 healthy men, using a double-blind cross-over design. After a run-in period on placebo of 1 week, the subjects were treated with either placebo (n = 6) or xipamide 20 mg once daily (n = 6) for 16 weeks and were then switched to the alternative medication for another 16 weeks. The plasma concentration of alpha-atrial natriuretic peptide fell after 1 week of xipamide administration and increased during prolonged xipamide administration but remained reduced. The changes in plasma alpha-ANP observed after 1 week of xipamide were negatively correlated with the changes in hematocrit and hemoglobin. Plasma renin activity (PRA), aldosterone concentration (PAC), and urinary excretion of aldosterone and kallikrein increased after 1 week of xipamide administration, levelled off during the second and fourth weeks, but remained elevated during further prolonged xipamide administration for 16 weeks. The xipamide-induced changes in PRA and PAC were positively correlated with the changes in the hematocrit and hemoglobin. The changes in plasma renin, aldosterone, and alpha-atrial natriuretic peptide during xipamide administration may be related to diuretic-induced volume contraction.
Cardiovasc Drugs Ther 1991 Aug
PMID:Hormonal effects of the diuretic xipamide in healthy men. 183 91

A total of 114 children (age range 4 months to 18 years) underwent definitive operation for life-threatening or incessant tachydysrhythmias resulting from accessory conduction pathways (Kent bundle) (79), atrial ectopic foci (18), or ventricular ectopic foci (17). Of the patients with the accessory pathway type of supraventricular tachycardia, 63.3% (50/79) had classical Wolff-Parkinson-White syndrome whereas 36.7% (29/79) had retrograde conduction only across the pathway. Locations of the pathways were as follows: left posterior 48.1% (38/79), right anterior or lateral 27.8% (22/79), posterior septal 16.5% (13/79), anterior septal 3.8% (3/79), and both right and left 3.8% (3/79). With increasing experience, the success rate (cure of tachycardia) improved from 85% in the first 40 patients to 95% in the last 40 patients. One surgical death (1.3%) occurred secondary to a paradoxical air embolus. Atrial ectopic tachycardia was treated by cryoablation (nine), excision (one), combined excision and cryoablation (six), and atrial disconnection (two). The ectopic focus was located on the right atrial wall in 13 patients (72.2%) and cardiopulmonary bypass was required in eight (44.4%). The operation was successful in 89%; two patients with multiple ectopic foci continued to have uncontrolled tachycardia after the operation. Ventricular tachycardia presenting in the first 2 years of life was due to gross tumor in three cases (rhabdomyoma two, fibroma one) or microscopic hamartomatous change (Purkinje tumor) in five cases and was treated by excision alone or with adjuvant cryoablation. In four cases no tumor was found but the area of ectopic focus was successfully cryoablated. One child with diffuse endocardial tumor died of low cardiac output after the operation. Ventricular tachycardia in older children was localized to outflow patch aneurysms or other areas in the right ventricle following tetralogy of Fallot repair (three patients, treated by excision or cryoablation) and arrhythmogenic right ventricular dysplasia (two patients, treated by right ventricular disconnection). We conclude that mapping and operation for supraventricular tachycardia resulting from accessory pathways are predictable and curative in a high percentage of patients. Atrial ectopic tachycardias are more difficult to precisely localize but can be cured by a combination of excisional and cryoablative techniques. Ventricular tachycardia in infants is lethal and is commonly due to ectopic foci or microscopic tumors that may not be apparent on preoperative angiography or echocardiography. Electrophysiologically directed operations in these patients can be lifesaving.
J Thorac Cardiovasc Surg 1985 Nov
PMID:Definitive operation for refractory cardiac tachyarrhythmias in children. 405 40

In a prospective randomized study we searched for arrhythmogenic effects of the tetracyclic antidepressant, a maprotiline, and the tetrahydroisoquinoline derivative, nomifensine. Forty depressive patients from the psychiatric outpatients department were included in the study. Twenty patients in each group received maprotiline or nomifensine over three weeks in the recommended daily dosage of 75 mg. Rhythm analysis was performed before therapy, at the end of 3 weeks therapy, and 1 week after withdrawal from medication using a dual channel long-term ECG with monitoring periods of 10 h during normal daily activities. Before treatment, spontaneous incidence of all ventricular ectopics and of their complex forms was within the normal range when compared with ectopic activity of 121 "normal subjects" without detectable heart disease. No significant increase could be demonstrated during therapy with maprotiline or nomifensine, nor was any change observed 1 week after medication had been stopped. The same was true for supraventricular extrasystoles; atrial tachycardia, atrial flutter, and fibrillation were never seen. Sinoatrial (n=2) and atrioventricular block (n=1) were rare findings independent of and not affected by treatment. No bundle branch blocks were observed before, during, and after treatment. In contrast, despite the conservative dosage of both drugs, a therapy-dependent increase in average heart rate was found (p less than 0.001). This increase was significantly higher in patients receiving nomifensine than in those treated with maprotiline (p less than 0.001), suggesting a lower intrinsic anticholinergic activity of the latter compound.
J Cardiovasc Pharmacol
PMID:Incidence of cardiac arrhythmias during antidepressant therapy with maprotiline or nomifensine. 617 91

We report initial successful results using a novel retrograde cutting (pullback) atherectomy catheter (PAC) to treat complex bifurcation coronary artery disease, in 2 patients. In one case a bifurcation lesion involving the left anterior descending and a large diagonal branch was treated without the need for two-wire or kissing-balloon technique. In the second case a high-grade eccentric lesion of the right coronary artery at the site of a right ventricular marginal branch was treated successfully. This report describes the first clinical application of pullback atherectomy in human coronary circulation, and suggests that this device may play a useful role in the treatment of complex bifurcation coronary artery disease.
Cathet Cardiovasc Diagn 1996 Jun
PMID:Pullback atherectomy (PAC) for the treatment of complex bifurcation coronary artery disease. 877 34

This study compared the effects of 1 year of monotherapy with a calcium-channel antagonist (nilvadipine; NIL), an angiotensin-converting enzyme (ACE) inhibitor (temocapril; TEM), or a new vasodilator (cadralazine; CAD) on left ventricular (LV) hypertrophy in essential hypertension. Furthermore, to elucidate the mechanism responsible for regression of LV hypertrophy after treatment, LV mass index (LVMI) by echocardiography, plasma renin activity (PRA), aldosterone (PAC), norepinephrine, and atrial natriuretic peptide (ANP) concentration were measured before and after treatment. Thirty-six patients were randomly assigned to the NIL, TEM, or CAD groups. Blood pressure (BP) before treatment was 174 +/- 10/104 +/- 7, 173 +/- 18/103 +/- 8, and 171 +/- 16/103 +/- 7 mm Hg (mean +/- SD) in NIL, TEM, and CAD groups, respectively. BP was lower after treatment with each of the three test drugs than after the placebo period, and there were no differences in BP reduction among three groups. LVMI, in NIL and TEM, was reduced from 129 +/- 48 to 115 +/- 39 g/m2 and from 117 +/- 39 to 88 +/- 20 g/m2 (p < 0.05 and p < 0.01, respectively), whereas, in the CAD group, it was increased (110 +/- 30 to 138 +/- 27 g/m2; p < 0.01). In the CAD group, PAC decreased and ANP increased significantly. The change in LVMI correlated with that in BP for TEM and with that in ANP in all patients. These data indicated that LV volume overload as well as LV pressure overload may contribute to LV hypertrophy and that monotherapy with CAD is not desirable from the point of view of LV mass reduction in essential hypertension.
J Cardiovasc Pharmacol 1997 Nov
PMID:The effects of long-term treatment on left ventricular hypertrophy in patients with essential hypertension: relation to changes in neurohumoral factors. 938 47

We examined if sevoflurane given before cold ischemia of intact hearts (anesthetic preconditioning, APC) affords additional protection by further improving mitochondrial energy balance and if this is abolished by a mitochondrial KATP blocker. NADH and FAD fluorescence was measured within the left ventricular wall of 5 groups of isolated guinea pig hearts: (1) hypothermia alone; (2) hypothermia+ischemia; (3) APC (4.1% sevoflurane)+cold ischemia; (4) 5-HD+cold ischemia, and (5) APC+5-HD+cold ischemia. Hearts were exposed to sevoflurane for 15 minutes followed by 15 minutes of washout at 37 degrees C before cooling, 2 hours of 27 degrees C ischemia, and 2 hours of 37 degrees C reperfusion. The KATP channel inhibitor 5-HD was perfused before and after sevoflurane. Ischemia caused a rapid increase in NADH and a decrease in FAD that waned over 2 hours. Warm reperfusion led to a decrease in NADH and an increase in FAD. APC attenuated the changes in NADH and FAD and further improved postischemic function and reduced infarct size. 5-HD blocked the cardioprotective effects of APC but not APC-induced alterations of NADH and FAD. Thus, APC improves redox balance and has additive cardioprotective effects with mild hypothermic ischemia. 5-HD blocks APC-induced cardioprotective effects but not improvements in mitochondrial bioenergetics. This suggests that mediation of protection by KATP channel opening during cold ischemia and reperfusion is downstream from the APC-induced improvement in redox state or that these changes in redox state are not attenuated by KATP channel antagonism.
J Cardiovasc Pharmacol 2005 Sep
PMID:Improved mitochondrial bioenergetics by anesthetic preconditioning during and after 2 hours of 27 degrees C ischemia in isolated hearts. 1611 32

Cyclo-oxygenase (COX) 1 mediates the production of thromboxane A2 in platelets, leading to platelet aggregation and vasoconstriction. Conversely, COX2 catalyzes endothelial prostacyclin synthesis, which effectively counteracts thromboxane A2, triggering vasodilation and platelet inhibition. Selective COX2 inhibitors decrease prostacyclin production, potentially disrupting homeostasis and creating a prothrombotic state. The VIGOR study findings of increased cardiovascular risk with rofecoxib were subsequently confirmed by large meta-analyses, observational studies and recent APPROVe trial publication. The APC trial findings of increased cardiovascular risk with Celebrex (celecoxib) conflict with those in the ADAPT trial, the upcoming PreSAP publication, a case-control study by Graham et al. and prior large clinical trials, meta-analyses and observational studies of this drug. Therefore, while an adverse class effect is a possibility for COX2 inhibitors, the published data are inconsistent. Baseline cardiovascular risk in patients might contribute significantly to these findings. In light of the negative Vioxx (rofecoxib) publicity, however, COX2 inhibitors might forever remain underinvestigated. The relative selectivity of these compounds for COX2 is extremely variable, casting significant doubt on the class-effect hypothesis. Improved endothelial function has also been reported with celecoxib, leading to endothelium-dependent vasodilation, and associated decreases in C-reactive protein and LDL cholesterol. The addition of meloxicam to low-dose aspirin and heparin has improved clinical outcomes after acute coronary syndromes. These are the first studies suggesting improvement in endothelial function and reduction of inflammation with COX2 inhibition. Thus, more randomized controlled trials are needed to study the relative cardiovascular effects of different COX2 inhibitors, alone and in combination with aspirin.
Nat Clin Pract Cardiovasc Med 2005 Jun
PMID:Drug insight: cyclo-oxygenase 2 inhibitors and cardiovascular risk--where are we now? 1626 33


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