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PubMed1995

Effects of hypertrophy on left atrial and ventricular compliance and plasma ANF levels in conscious dogs.

Alterations in left atrial (LA) and left ventricular (LV) compliance and arterial and coronary sinus atrial natriuretic factor (ANF) concentrations at baseline and in response to both volume depletion and expansion were investigated in 15 conscious dogs with aortic banding-induced LV hypertrophy (LVH) (LV/body wt increased by 64%), which also induced LAH (LA/body wt increased by 61%). With volume expansion coronary sinus ANF increased more (P < 0.05) in dogs with LVH (+427 +/- 88 pg/ml) compared with control dogs (+146 +/- 45 pg/ml). Arterial ANF levels also rose more with volume expansion in LVH. In dogs with LVH, the LV end-diastolic pressure-diameter relationship was shifted to the left with a steeper slope with volume expansion, such that at any given diastolic dimension, diastolic pressure was higher. In contrast, the pressure-dimension relationship for the LA appendage was shifted in the opposite direction during both atrial systolic and diastolic phases, with a more shallow slope in hypertrophy compared with control dogs, resulting in an augmented pressure-dimension product during volume loading in LAH. In conclusion, in dogs with LVH and LAH, enhanced ANF was revealed in the coronary sinus and systemic circulation during volume expansion, which could be due, in part, to a more compliant, but hypertrophied, LA, which responded to equivalent volume loading with an augmented pressure-dimension product.

Animals↗
PubMed2004

Effects of enhanced external counterpulsation on hemodynamics and its mechanism.

BACKGROUND: The hemodynamic effects of enhanced external counterpulsation (EECP) and its mechanism(s) were investigated in relation to neurohumoral factors in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Twenty-four patients with AMI were studied before, during and after EECP treatment for 60 min. Heart rate (HR), right atrial pressure (RAP), pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) were determined. In addition, circulating concentrations of neurohumoral factors were determined at each time point. HR did not change following EECP treatment. However, RAP and PCWP increased significantly and CI was significantly elevated during EECP and thereafter. Blood atrial natriuretic peptide (ANP) concentration was significantly increased 15 and 60 min after the start of EECP treatment, but brain natriuretic peptide (BNP) did not change. Renin, aldosterone and catecholamine concentrations also did not change. CONCLUSION: Treatment with EECP resulted in an increased preload because of increased venous return, and CI was increased thereafter. In patients with AMI, EECP increased blood ANP concentration, but not BNP, which suggests that an increase in ANP without an increase in BNP is an important mechanism for the effects of EECP treatment.

Aged↗
PubMed1983

Prolapse of the mitral valve in secundum atrial septal defect: a functional mechanism.

Prolapse of the mitral valve in patients with secundum atrial septal defect has been described angiographically and by two-dimensional echocardiography. It has been suggested that prolapse of the mitral valve in these patients is due to distortion of left ventricular shape and small left ventricular volume. To test this hypothesis 10 patients with unrepaired secundum atrial septal defect and 10 patients who had undergone repair of the defect were studied by two-dimensional echocardiography. The prevalence of mitral valve prolapse was 80% in the unrepaired group and 20% in the repaired group (P less than 0.01). Short axis of the left ventricle revealed septal bulging into the left ventricle, the end-diastolic ratio of minor to major axis being 0.71 in the unrepaired group and 0.93 in the repaired group (P less than 0.001). Systolic and diastolic cross-sectional areas were larger in the repaired group compared with the unrepaired group (P less than 0.05). Prolapse of the mitral valve in patients with secundum atrial septal defect may be related to the distorted left ventricular shape and small left ventricular volume.

Adolescent↗
PubMed1976

The contribution of atrial contraction to right heart function before and after right ventriculotomy. Experimental and clinical observations.

Effective atrial contraction was abolished by simultaneous atrial and ventricular (A-V) pacing in an acute canine preparation. At constant cardiac output, aortic pressure, and heart rate, only a small rise (1.4 mm. Hg) in mean right atrial pressure was observed before vertical right ventriculotomy, but a larger rise (9.5 mm Hg) occurred after ventriculotomy (p less than 0.01). Right heart failure with tricuspid regurgitation was induced after ventriculotomy by volume overload and A-V pacing. Restoration of atrial contraction (sequential A-V pacing) eliminated regurgitation and lowered average mean right atrial pressure from 22 to 4 mm. Hg (p less than 0.001). After right ventriculotomy, loss of atrial contraction at a constant right atrial pressure resulted in a 42 per cent reduction in cardiac output. In 8 patients who had had right ventriculotomies, abolition of effective atrial contraction by A-V pacing caused an average reduction in cardiac output of 22 per cent, whereas cardiac output fell only 5 per cent in 5 control patients (p less than 0.01).

Animals↗
PubMed1993

Plasma brain natriuretic peptide and atrial natriuretic peptide concentrations correlate with left ventricular end-diastolic pressure.

The present study was designed to investigate whether brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations correlate with left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), diastolic pulmonary arterial pressure (DPAP), right atrial pressure (RAP), or ejection fraction (EF). Plasma BNP and ANP levels were determined by commercial radioimmunoassays (Peninsula) after Sep Pak C18 extraction in blood samples withdrawn from the pulmonary artery and the left ventricle or from the left ventricle and the femoral vein in 85 patients undergoing diagnostic cardiac catheterization. Linear and nonlinear regression analysis and the paired sample t-test were applied to the data. Pulmonary arterial plasma BNP and ANP levels showed a close nonlinear correlation with LVEDP (BNP: r = 0.94, p < 0.001; ANP: r = 0.81, p < 0.001), a significant linear correlation with PCWP, DPAP, and RAP, and a significant negative correlation with EF. ANP concentrations decreased significantly from the pulmonary artery to the left ventricle and from the left ventricle to the femoral vein (p < 0.001). BNP levels also decreased significantly between the left ventricle and the femoral vein (p < 0.001), but there was no significant difference between pulmonary arterial and left ventricular BNP concentrations. BNP and ANP concentrations correlated significantly between pulmonary arterial and left ventricular blood samples (BNP: r = 0.99, ANP: r = 0.93, p < 0.001) and between left ventricular and peripheral blood samples (BNP: r = 0.99, ANP: r = 0.94, p < 0.001). The present data suggest that peripheral plasma BNP and ANP levels are useful non-invasive indices of cardiac performance.

Atrial Function, Right↗
PubMed2006

Kv1.5 channelopathy due to KCNA5 loss-of-function mutation causes human atrial fibrillation.

Atrial fibrillation is a rhythm disorder characterized by chaotic electrical activity of cardiac atria. Predisposing to stroke and heart failure, this common condition is increasingly recognized as a heritable disorder. To identify genetic defects conferring disease susceptibility, patients with idiopathic atrial fibrillation, lacking traditional risk factors, were evaluated. Genomic DNA scanning revealed a nonsense mutation in KCNA5 that encodes Kv1.5, a voltage-gated potassium channel expressed in human atria. The heterozygous E375X mutation, present in a familial case of atrial fibrillation and absent in 540 unrelated control individuals, introduced a premature stop codon disrupting the Kv1.5 channel protein. The truncation eliminated the S4-S6 voltage sensor, pore region and C-terminus, preserving the N-terminus and S1-S3 transmembrane domains that secure tetrameric subunit assembly. Heterologously expressed recombinant E375X mutant failed to generate the ultrarapid delayed rectifier current I(Kur) vital for atrial repolarization and exerted a dominant-negative effect on wild-type current. Loss of channel function translated into action potential prolongation and early after-depolarization in human atrial myocytes, increasing vulnerability to stress-provoked triggered activity. The pathogenic link between compromised Kv1.5 function and susceptibility to atrial fibrillation was verified, at the organism level, in a murine model. Rescue of the genetic defect was achieved by aminoglycoside-induced translational read-through of the E375X premature stop codon, restoring channel function. This first report of Kv1.5 loss-of-function channelopathy establishes KCNA5 mutation as a novel risk factor for repolarization deficiency and atrial fibrillation.

Animals↗
PubMed2002

The electromechanical effects of pacing at different sites within the right atrium.

AIMS: To compare high right atrium (HRA) with right atrial appendage (RAA) pacing with respect to atrial electromechanical function. METHODS: Eleven patients undergoing elective electrophysiological studies were studied in order directly to compare atrial conduction acutely associated with HRA and RAA pacing. Twenty-five patients with chronically implanted, active fixation leads in the HRA were compared with an age and sex matched group of 25 patients with chronically implanted, passive fixation leads in the RAA. For both studies recordings were taken in sinus rhythm then repeated when paced. Measured time intervals were intra- and interatrial activation times. P wave duration and time to onset of atrial systolic blood flow. RESULTS: Right atrial pacing, when compared with sinus rhythm, significantly prolongs the interatrial activation time, the P wave duration and the time to onset of right and left atrial blood flow irrespective of site paced. Comparing the RAA group with the HRA group, there were no statistical differences for any of the measured parameters. CONCLUSION: High right atrial free wall or the right atrial appendage pacing, when compared with sinus rhythm, is significantly detrimental to atrial electromechanical function. There is, however, no demonstrable difference between the two sites.

Adult↗
PubMed2006

Relationship between left atrial and left ventricular function in hypertrophic cardiomyopathy: a real-time 3-dimensional echocardiographic study.

BACKGROUND: Left atrium (LA) in patients with hypertrophic cardiomyopathy (HC) has been known to have an increased size and decreased contractile function. The purpose of this study was to investigate LA and left ventricular (LV) volume change and function with real-time 3-dimensional (3D) echocardiography and to investigate association between LA and LV function in HC. METHODS: We performed real-time 3D echocardiography on 26 patients with HC and on 15 control subjects. LA and LV time-volume curves were obtained from real-time 3D echocardiography and the maximal slope of the time-volume curve was expressed as dV/dt. LA active emptying fraction was calculated as: [(precontraction LA volume - minimal LA volume)/precontraction LA volume] x 100. RESULTS: The maximal LA volume index was larger, and LA active emptying fraction was lower, in those with HC than control subjects (50.1 +/- 15.9 vs 30.1 +/- 6.8 mL/m(2) and 33.3 +/- 13.7 vs 40.4 +/- 8.6%, both P< .05). LA active emptying fraction showed a negative correlation with precontraction LA volume (r = -0.64, P < .01) in HC. Patients with HC showed decreased LV early diastolic dV/dt compared with control subjects (0.10 +/- 0.05 vs 0.14 +/- 0.04 mL/ms, P < .05). LA passive and active emptying dV/dt were correlated with LV early and late diastolic dV/dt, respectively (r = 0.47 and r = 0.48, both P < .05). CONCLUSION: Our 3D echocardiographic study showed that increased LA volume was related to decreased LA contraction in HC. LA passive emptying was related to LV relaxation whereas LA active contraction was related to LV stiffness.

Adult↗
PubMed1991

Atrial natriuretic peptide responses during anaesthesia in patients with refractory cardiomyopathies.

In patients with congestive heart failure, the release of atrial natriuretic peptide (ANP) is decreased. This study sought to determine the extent of ANP, sympathetic and haemodynamic responses to acutely increased atrial pressure in patients with cardiomyopathies undergoing orthotopic cardiac transplantation. Haemodynamic variables, plasma ANP, norepinephrine, and epinephrine concentrations were measured in 17 patients at five times before and after induction of anaesthesia using either ketamine 1.5 micrograms.kg-1 or sufentanil 3.6 +/- 0.3 micrograms.kg-1. Preinduction values in the ketamine and sufentanil groups were not significantly different. Compared with preinduction values, increases in mean arterial pressure (26%), pulmonary capillary wedge pressure (90%), right atrial pressure (107%), and heart rate (24%) occurred in the ketamine group while cardiac index decreased by 19% (P less than 0.05). Haemodynamic variables in the sufentanil group did not change at any of the times studied. Plasma concentrations of atrial natriuretic peptide were not different within or between treatment groups. Following tracheal intubation plasma norepinephrine levels increased by 116% in the ketamine group (P less than 0.05), but did not change in the sufentanil group. Plasma norepinephrine concentrations differed significantly between the ketamine and sufentanil groups. There were no differences in epinephrine concentrations in either group. Despite the anticipated haemodynamic and catecholamine differences found between the ketamine and sufentanil groups, the levels of plasma ANP were similar. Based upon these results, it is concluded that ANP exerts little influence in the control of fluid volume or blood pressure in patients with refractory cardiomyopathy.

Adult↗
PubMed1993

Acute and delayed hormonal changes in mitral stenosis treated by balloon valvulotomy.

The role of left atrial and aortic pressures on the secretion of the main hormones controlling blood volume is still subject to debate in humans. Because of increased mean left atrial pressure and decreased mean aortic pressure produced by balloon inflation in patients with mitral stenosis treated with balloon valvulotomy, the hormonal changes occurring acutely (group II of patients) were measured. The same studies (group I patients) were also performed 48 hours after this treatment, a period at which left atrial pressure permanently diminished. Inflation of the balloon resulted in a decrease in plasma renin activity and increases in plasma atrial natriuretic factor (ANF) and plasma arginine vasopressin (AVP). Forty-eight hours after balloon valvulotomy, which had produced a decrease in left atrial pressure, plasma ANF was lower (58.9 +/- 7.9 vs 95.3 +/- 11.9 pg/ml; p < 0.001), and plasma renin activity (2,575 +/- 533 vs 960 +/- 113 pg/ml/hour; p < 0.01), plasma angiotensin II (25.0 +/- 4.1 vs 9.3 +/- 1.3 pg/ml; p < 0.001) and plasma aldosterone (181.7 +/- 36.7 vs 139.9 +/- 19.8 pg/ml; p < 0.05) were higher than their respective control levels 24 hours before treatment of the stenosis. In contrast, plasma AVP (3.7 +/- 0.25 vs 4.4 +/- 0.31 pg/ml; p = 0.001) diminished moderately along with plasma osmolality (282.4 +/- 0.1 vs 286.2 +/- 0.6 mOsm/kg; p < 0.001). Urinary sodium excretion was also examined before and after balloon valvulotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Fumarate-enriched blood cardioplegia results in complete functional recovery of immature myocardium.

Amino acid enrichment of cardioplegic solutions has been shown to improve both the metabolic and functional recovery of ischemic myocardium. However, because of the marked systemic vasodilatation involved, use of amino acid enrichment is limited to the periods of induction and reperfusion. Fumarate is a Krebs' cycle intermediate whose conversion to succinate is responsible for the generation of adenosone triphosphate and the oxidation of the reduced form of nicotinamide-adenine nucleotide which is the pathway by which aspartate exerts its effect. Fumarate may also function as a free-radical scavenger and is involved in calcium transport. To determine if fumarate-enriched blood cardioplegia would improve the functional recovery of the neonatal heart, 14 neonatal piglet hearts were isolated and placed on a blood-perfused working heart circuit. After the baseline functional and metabolic assessment was done, cold ischemic arrest was initiated with either standard blood cardioplegic solution (group I; N = 7) or fumarate-enriched (13 mmol/L) blood cardioplegic solution (group II; N = 7). Cardioplegic solution was given at a pressure of 40 mm Hg every 20 minutes for 2 hours, and topical hypothermia was used. Sixty minutes after warm whole blood reperfusion, the functional recovery at left atrial pressures of 3, 6, 9, and 12 mm Hg was 70%, 66%, 66%, and 65%, respectively, in group I, versus 102%, 106%, 105%, and 109%, respectively, in group II (p < 0.05). The tissue creatinine phosphate levels after reperfusion were significantly higher in group II hearts (15.0 +/- 1.2 mumol/g dry heart tissue) than in group I hearts (9.2 +/- 1.9 mumol/g dry heart tissue), although the adenosine triphosphate levels were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1993

The influence of reproductive hormones on ANF release by rat atria.

The effects of subcutaneous (sc) administration of estradiol (50 micrograms/100 microliters/day x 10 day) or testosterone (15 mg/100 microliters twice a week x 2 weeks) on ANF release were examined in isolated perfused rat atria. The concentration of ANF in the perfusate was measured by radioimmunoassay, under basal conditions (atrial wall unstressed), and during atrial distention (intraluminal pressure raised to 4, 6, and 10 cm water). In both male and female control (vehicle-injected) groups, increased atrial pressure resulting in distention of the atrium caused a significant increase in ANF release. Estradiol increased basal secretion of ANF but did not influence stretch-induced stimulation of ANF secretion. By contrast, although testosterone did not affect basal secretion, it completely abolished the stretch-induced increase in ANF secretion. Neither estradiol nor testosterone affected atrial compliance.

Animals↗
PubMed1992

Right atrial predominance of atrial natriuretic peptide secretion in isolated perfused rat atria.

In order to investigate the regulatory mechanism for the atrial release of atrial natriuretic peptide (ANP), a perfused rabbit atrial model was devised. In the present experiments, the effect of a reduction in atrial distension on the immunoreactive ANP (irANP) secretion was investigated and compared in the perfused right and left atria of rats. Elevations in right and left atrial pressure resulted in proportional increases in the volume of atrial distension-reduction which was larger in the right than in the left atria. The basal rate of irANP secretion was higher in the right than in the left atria. Increases in the volume of atrial distension-reduction resulted in proportional increases in irANP secretion in both atria. Increment in irANP secretion in response to a reduction in atrial distension was significantly higher in the right than in the left atria. Higher rate of irANP secretion in response to unit volume change was observed in the right atria. Increases in the volume of atrial distension-reduction resulted in accentuated irANP responses in the right atrium. IrANP content was significantly higher in the right than in the left atria. The results suggest that the right atrium is a predominant site in ANP secretion in rats.

Animals↗
PubMed1994

Response of atrial natriuretic factor to surgical pericardial drainage in patients with chronic pericardial effusion.

Previous studies have demonstrated the importance of atrial transmural pressure in the secretion of atrial natriuretic peptide. These studies have been performed in patients with pericardial effusion and hemodynamic compromise. The response of atrial natriuretic peptide to the drainage of chronic pericardial effusion without clinical evidence of tamponade is unknown. We studied 13 patients with chronic abundant pericardial effusion but without hemodynamic compromise. Blood samples for hormonal determinations were drawn before and after surgical pericardiocentesis. Right atrial pressure was measured during the procedure. Drainage induced a significant increase of atrial natriuretic peptide (from 12 +/- 3.9 to 105 +/- 22.8 pmol/l, P < 0.001, mean +/- S.E.M.), correlated with the fall in right atrial pressure (from 7.65 +/- 1.18 to 4.31 +/- 1.46 mmHg, P < 0.05, r = 0.68, P = 0.01). This increase was inversely correlated with the rise of mean blood pressure after surgery (from 84 +/- 2.37 to 100 +/- 5.3 mmHg, P < 0.05, r = 0.65, P < 0.02). Plasma renin activity decreased after drainage (from 8.12 +/- 2.57 to 3.27 +/- 0.65 ng/ml/h, P < 0.05). Surgery induced an increase of plasma levels of aldosterone (from 811 +/- 241 to 1199 +/- 249 pmol/l, P < 0.05), which were reduced after pericardiocentesis (371 +/- 102 pmol/l, P < 0.02). In patients with chronic abundant pericardial effusion, surgical pericardiocentesis induced a significant increase of atrial natriuretic peptide, correlated with a fall in right atrial pressure. The increase of atrial natriuretic peptide was similar than in patients with tamponade, despite a moderate fall in right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

In vivo electrophysiological effects of a selective slow delayed-rectifier potassium channel blocker in anesthetized dogs: potential insights into class III actions.

OBJECTIVES: This study evaluated the in vivo electrophysiological effects of a highly selective slow delayed-rectifier K+-current blocker, HMR 1556, to gain insights into the consequences of selectively inhibiting the slow delayed-rectifier current in vivo. METHODS: Atrial and ventricular effective refractory periods, sinus node recovery time, Wenckebach cycle-length, atrial fibrillation duration and electrocardiographic intervals were measured before and after intravenous HMR 1556. RESULTS: HMR 1556 increased atrial and ventricular refractory periods (e.g. by 6 +/- 4% and 27 +/- 6% at cycle lengths of 360 and 400 ms, respectively), QT intervals and sinus-node recovery times. Beta-adrenoceptor blockade with nadolol abolished all effects except those on ventricular refractoriness and changed positive use-dependent effects on refractoriness to reverse use-dependent ones. In the presence of dofetilide to block rapid delayed-rectifier current, HMR 1556 effects were potentiated (e.g. atrial and ventricular refractory periods increased by 26 +/- 3% and 34 +/- 3% at cycle lengths of 360 and 400 ms, respectively). HMR 1556 reduced vagal atrial fibrillation duration from 1077 +/- 81 to 471 +/- 38 s, an effect abolished by nadolol and greatly potentiated by dofetilide (duration 77 +/- 30 s). HMR 1556 increased Wenckebach cycle length only in the presence of dofetilide. CONCLUSIONS: Slowed delayed-rectifier current inhibition affects atrial repolarization, sinus node function and atrial fibrillation in vivo, but only in the presence of intact beta-adrenergic tone, and delays ventricular repolarization even when beta-adrenoceptors are blocked. The slow delayed-rectifier current is particularly important when rapid delayed-rectifier current is suppressed, illustrating the importance of repolarization reserve.

Adrenergic beta-Antagonists↗
PubMed2006

Augmentation of insulin-stimulated ANP release through tyrosine kinase and PI 3-kinase in diabetic rats.

The aim of present study was to define the effects of insulin on atrial dynamics and ANP release and its modification in diabetic rats. An isolated perfused beating atrial model was used from control and diabetic rats. Insulin was perfused with and without an inhibitor for tyrosine kinase or phosphatidylinositol 3-kinase (PI 3-kinase). Insulin increased the release of ANP and decreased atrial contractility in a dose-dependent manner. During the perfusion of 10(-10)M insulin, the release of ANP abruptly increased within 8min by approximately 40% and then decreased with time despite of continuous perfusion. In terms of increasing the dose of insulin, the time to reach the peak effect became faster and the slope to decrease became slower. In contrast, atrial contractility was gradually decreased with time. These effects were independent upon extracellular glucose. Genistein (10(-5)M) or lavendustin C (10(-5)M), a tyrosine kinase inhibitor, attenuated the release of ANP stimulated by insulin (10(-8)M). Wortmannin (10(-7)M) or LY294002 (10(-5)M), a PI 3-kinase inhibitor, also attenuated insulin-stimulated ANP release. However, both inhibitors for PI 3-kinase and tyrosine kinase did not cause any significant effects on negative inotropism by insulin. Insulin-stimulated ANP release was augmented in streptozotocin-treated rat atria. The density of insulin receptor markedly increased in diabetic hearts. These results suggest that insulin stimulates the release of ANP through PI 3-kinase and tyrosine kinase, and augmentation of insulin-stimulated ANP release in diabetic rat atria may be partly due to an upregulation of insulin receptor.

Animals↗
PubMed2000

Clinical, echocardiographic, and hormonal factors influencing spontaneous conversion of recent-onset atrial fibrillation to sinus rhythm.

The present study was designed to determine clinical, hormonal, and echocardiographic factors influencing spontaneous conversion to sinus rhythm of recent-onset atrial fibrillation (symptoms <6 hours). The most important predictor of spontaneous conversion was the time of onset of atrial fibrillation; patients who developed the arrhythmia during sleep had the highest probability of spontaneous conversion during the first 24 hours. A second predictor was the plasma concentration of atrial natriuretic peptide during the arrhythmia.

Adult↗
PubMed2003

Atrial fibrillation: hypertension as a causative agent, risk factor for complications, and potential therapeutic target.

Atrial fibrillation and hypertension are 2 prevalent, and often coexistent, conditions in the North American population. Their incidence increases with advancing age, and they are responsible for considerable morbidity and mortality. Although the relation between the 2 conditions has long been known, the treatment of hypertension is not currently a focus in the clinical management of atrial fibrillation. Hypertension is associated with left ventricular hypertrophy, impaired ventricular filling, left atrial enlargement, and slowing of atrial conduction velocity. These changes in cardiac structure and physiology favor the development of atrial fibrillation, and they increase the risk of thromboembolic complications. Conventional therapy of atrial fibrillation has focused on interventions to control heart rate and rhythm and the prevention of stroke through the use of anticoagulant medications. In patients with atrial fibrillation, aggressive treatment of hypertension may reverse the structural changes in the heart, reduce thromboembolic complications, and retard or prevent the occurrence of atrial fibrillation. Specific pharmacotherapy could potentially play a major role in the primary and secondary prevention of atrial fibrillation and its complications.

Antihypertensive Agents↗