Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “atrial function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources

The treatment of atrial fibrillation. An evaluation of drug therapy, electrical modalities and therapeutic considerations.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in clinical practice, and is responsible for considerable morbidity. Basic studies have shown that AF is usually due to the coexistence of multiple functional atrial re-entry circuits, and that the main determinant of its haemodynamic manifestations is the ventricular response rate. The major adverse clinical consequences of AF include palpitations, impaired cardiac function and thromboembolism. One approach to treating AF is to convert the patient's cardiac rhythm to sinus rhythm by direct current electrical cardioversion, which is initially successful in about 90% of cases. However, the AF recurrence rate over the year subsequent to cardioversion is very high, in the order of 75% in patients receiving no drug therapy. Class I and class III antiarrhythmic drugs reduce the rate of recurrence of AF, but at the expense of a variety of potential adverse effects including ventricular proarrhythmia. The latter is a rare effect (occurring in 1 to 2% of patients receiving most drugs), but can be lethal. A second approach to therapy is to leave the patient in AF, but to control the ventricular response rate and to prevent thromboemboli with oral anticoagulants. Disadvantages of this approach include the possibilities of functional limitations imposed by the arrhythmia, adverse effects of drug therapy, and major bleeding related to anticoagulation. New approaches currently under study include surgery to prevent AF from sustaining itself, implantable cardioverter devices to maintain sinus rhythm, and modification of AV nodal function by the induction of controlled radiofrequency injury.

Animals↗

Proarrhythmic and antiarrhythmic effects of intravenous prostacyclin in man.

Prostacyclin (PGI2) has been shown to reduce the occurrence of experimental ventricular arrhythmias. To assess potential beneficial effects in man, the electrophysiological action of PGI2 was studied in 16 non medicated patients. The protocol used in incremental pacing and programmed stimulation in the right atrium and ventricle. This protocol and measurement of effective refractory periods (ERP) were performed before and during the injection of 2.5, 5 and 10 ng kg-1 min-1 of PGI2. The atrial functional refractory period decreased significantly (P less than 0.05); PGI2 had no influence on the occurrence of inducible non-sustained (NS) atrial tachycardias and was responsible for the occurrence of 2 non-sustained atrial tachycardias in 8 patients with inducible atrial echo beats under basal conditions. Thirteen patients did not have inducible ventricular tachycardia (VT) under basal conditions. Non-sustained VT was induced after PGI2 in 4 of them but in only 1 of them after the administration of propranolol. Three patients had inducible VT under basal conditions (1 non-sustained, 2 sustained VT). PGI2 did not prevent the occurrence of VT (1 non-sustained, 1 sustained VT), except in 1 patient with ischaemic-related VT, who had non-sustained VT after PGI2. In conclusion, PGI2 does not seem to have a cardiac antiarrhythmic effect and may increase the atrial and ventricular repetitive response. This effect could be related to an increase of adrenergic tone.

Adult↗

Quantification of atrial tachyarrhythmia burden with an implantable pacemaker before and after pulmonary vein isolation.

Long-term efficacy of pulmonary vein (PV) ostial isolation for paroxysmal atrial fibrillation is difficult to assess. We evaluated the net duration of atrial tachyarrhythmia episodes (burden), atrial tachyarrhythmia episode frequency, and quality-of-life (QOL) before and after PV isolation in patients with an existing pacemaker featuring extensive diagnostic capabilities. Due to frequent recurrences of paroxysmal atrial fibrillation, PV isolation was performed 21 +/- 10 months following pacemaker implantation on 12 patients (57 +/- 5 years) with normal left ventricular function. Atrial tachyarrhythmia burden (ATB) and episode frequency were monitored daily by the device both pre- and postablation. QOL questionnaires were collected at ablation and 1, 3, and 6 months thereafter. Patients were followed for 20 +/- 9 and 11 +/- 9 months pre- and postablation, respectively. Membrane-active antiarrhythmic medications were discontinued after ablation in 8 of 12 patients. PV isolation resulted in a significant reduction of ATB from a median of 3.2 hours/day (preablation) to 0.2 hours/day (postablation, P < 0.01, Wilcoxon signed-rank test). The median tachyarrhythmia frequency was 6.4 episodes/day (preablation) and 0.3 episodes/day (postablation, P = 0.09). QOL measures significantly improved over the data collection intervals (P < 0.05). Tachyarrhythmia burden was positively associated with Symptom Checklist frequency and severity (P < 0.01). Significant long-term reductions in total ATB (symptomatic and asymptomatic) were observed. Furthermore, reductions in ATB were associated with improvements in QOL measures. Extensive monitoring capabilities in implantable devices help provide complete disclosure on the effect of PV isolation in paroxysmal atrial fibrillation patients.

Atrial Fibrillation↗

Right atrial MR imaging studies of cadaveric atrial casts and comparison with right and left atrial volumes and function in healthy subjects.

PURPOSE: To assess magnetic resonance (MR) imaging of the right atrium by measuring volumes of right atrial casts and determining right atrial volume cycles in healthy subjects. MATERIALS AND METHODS: Fourteen human cadaveric atrial casts were imaged and right atrial volumes of eight subjects were measured with cardiac-gated cine MR. Volumes were calculated and right and left atrial volumes were compared. RESULTS: Measured volumes of right atrial casts correlated well (r = .99, P < .001) with true volumes with a small underestimation noted (-7.2 mL +/- 2.3 [standard deviation], P < .001). The maximum in vivo right atrial volume averaged 77 mL/m2 +/- 11 of body area. The right atrial reservoir and conduit functions accounted for, on average, 58% and 19%, respectively, of the ventricular stroke volume; the remaining 23% came from atrial contraction. Right-to-left peak volume ratio averaged 1.41 +/- 0.15 (P < .001), and all volume measurements except conduit volumes were statistically significantly larger in the right atrium than the left. CONCLUSIONS: MR imaging provides a reliable means to study right atrial volumes and phasic function.

Adult↗

[Reduction of atrial fibrillation. New concepts, new strategies].

Restoring sinus rhythm is patients with non-valvular atrial fibrillation has two objectives: restore haemodynamic performance and reduce the risk of thromboembolism. Whether the cardioversion is spontaneous or induced with drugs or electroshock, the process itself carries the risk of systemic embolism attributed to the transitory inactivity of the left atrium. Current practice of giving anticoagulants at least 4 weeks before electric cardioversion is a compromise between the embolic risk of cardioversion estimated at 0.4 to 0.8% and haemorrhagic complications related to low blood coagulability estimated at about 1% per year. The advent of transoesophageal echography has made it possible to study the atrium in detail in search of thrombi. The result has been a revolution in our concepts and therapeutic approach to atrial fibrillation and cardioversion. Recent studies have shown that "rapid cardioversion" associated with minimal 48-hour anticoagulation with heparin IV and transoesophageal echography to eliminate a thrombus in the atrium and/or the atrial appendage can be proposed without increasing the risk of embolism. Besides simplifying the therapeutic protocols (but at the cost of the semiinvasive nature of the transoesophageal echocardiography), this method also has the merit of restoring atrial function rapidly, particularly in cases of recent onset arrhythmia.

Atrial Fibrillation↗

[Idiopathic atrial fibrillation of recent onset and atrial stunning: the echocardiographic evidence after pharmacological cardioversion].

Successful cardioversion of atrial fibrillation may result in prolonged recovery of normal atrial mechanical function. This prolonged recovery of atrial contraction (so-called atrial stunning) might depend on: the amount of energy delivered during direct current cardioversion; the time course between the onset of atrial fibrillation and the conversion to sinus rhythm; the size of the left atrium; the underlying cardiac disease. The aim of this study was to evaluate, in subjects with normal atrial size and without heart disease, the phenomenon of atrial stunning soon after pharmacological cardioversion of an episode of atrial fibrillation of recent onset. Twenty-five patients with an acute episode of atrial fibrillation, without evidence of heart disease and M-mode left atrial dimension (< or = 40 mm received i.v. propafenone or flecainide 2 mg/kg/10 min in order to restore sinus rhythm. Atrial fibrillation lasted < 48 hours in all patients. Doppler echocardiography was used to assess atrial function, by recording the peak velocity of atrial contraction (A wave). An echocardiographic study was performed within 12 hours of successful cardioversion and was repeated on day 3, 12 and 30. The size of the left atrium (37 +/- 3.9; 37.57 +/- 2.9; 37.4 +/- 4; 37.82 +/- 3.7 mm) and peak E velocity (57.97 +/- 18.3; 59.4 +/- 18.3; 59.0 +/- 16; 59.07 +/- 16.7 cm/s) did not show any significant differences over the time, as demonstrated by the serial echocardiographic evaluations. In contrast, both peak A velocity (cm/s) and E/A ratio evaluated within 12 hours of cardioversion (60.29 +/- 12.3 and 1.0 +/- 0.37) and on day 3 (73.71 +/- 10.7 and 0.82 +/- 0.27) were statistically different (p < 0.000001 and p < 0.00001). No further statistically significant increase was found in subsequent examinations (respectively 76.31 +/- 12 and 0.78 +/- 0.24 on day 12, and 76.91 +/- 14.8 and 0.78 +/- 0.21 on day 30). In conclusion, this study suggests that patients with alone atrial fibrillation of recent onset have a delayed recovery of normal atrial systolic function even after pharmacological cardioversion.

Adult↗

Effect of whiskey on atrial vulnerability and "holiday heart".

Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.

Adult↗

Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes.

Application of the current-clamp technique in rainbow trout atrial myocytes has yielded resting membrane potentials that are incompatible with normal atrial function. To investigate this paradox, we recorded the whole membrane current (I(m)) and compared membrane potentials recorded in isolated cardiac myocytes and multicellular preparations. Atrial tissue and ventricular myocytes had stable resting potentials of -87 +/- 2 mV and -83.9 +/- 0.4 mV, respectively. In contrast, 50 out of 59 atrial myocytes had unstable depolarized membrane potentials that were sensitive to the holding current. We hypothesized that this is at least partly due to a small slope conductance of I(m) around the resting membrane potential in atrial myocytes. In accordance with this hypothesis, the slope conductance of I(m) was about sevenfold smaller in atrial than in ventricular myocytes. Interestingly, ACh increased I(m) at -120 mV from 4.3 pA/pF to 27 pA/pF with an EC(50) of 45 nM in atrial myocytes. Moreover, 3 nM ACh increased the slope conductance of I(m) fourfold, shifted its reversal potential from -78 +/- 3 to -84 +/- 3 mV, and stabilized the resting membrane potential at -92 +/- 4 mV. ACh also shortened the action potential in both atrial myocytes and tissue, and this effect was antagonized by atropine. When applied alone, atropine prolonged the action potential in atrial tissue but had no effect on membrane potential, action potential, or I(m) in isolated atrial myocytes. This suggests that ACh-mediated activation of an inwardly rectifying K(+) current can modulate the membrane potential in the trout atrial myocytes and stabilize the resting membrane potential.

Acetylcholine↗

Long-term effect of VVI pacing on atrial and ventricular function in patients with sick sinus syndrome.

We conducted a prospective, 6-month echocardiographic study on the effect of VVI pacing on left atrial and ventricular function and dimensions in patients with sick sinus syndrome. Thirty-nine patients (23 women and 16 men, aged 71 +/- 9.2 years; 30 in sinus rhythm and 9 in atrial fibrillation) who had a VVI pacemaker implanted because of sick sinus syndrome were recruited in the study. In 26 patients who presented with and remained in sinus rhythm, paced left ventricular ejection fraction and stroke volume were significantly decreased (71.4% +/- 11.8% to 67.0% +/- 13.6%, and 73.9 +/- 29.0 cm3 to 66.3 +/- 21.1 cm3, respectively, P < 0.001 for both), whereas the paced diastolic dimension of the left atrium was significantly increased (3.2 +/- 0.7 cm to 3.7 +/- 0.9 cm, P < 0.001) at 6 months as compared with preimplantation. In nine patients with atrial fibrillation at implantation paced left ventricular ejection fraction at follow-up was significantly decreased (67.7% +/- 10.1% to 64.2% +/- 10.6%, P =0.003), but paced stroke volume and left atrial diastolic dimension were not significantly changed (75.1 +/- 25.6 cm3 to 79.0 +/- 22.7 cm3, and 4.3 +/- 1.2 cm to 4.6 +/- 1.5 cm, P = NS for both) at follow-up. Cessation of pacing and restoration of sinus rhythm in 21 patients at follow-up did not result in any significant change of ejection fraction (67.5% +/- 10.2% ti 67.6% +/- 9.7%, P = NS) whereas stroke volume was increased (59.1 +/- 19.6 cm3 to 69.1 +/- 22.3 cm3, P < 0.0001) in comparison with paced values. However, compared with preimplantation values, ejection fraction was significantly decreased (70.4% +/- 10.0% to 67.6% +/- 9.7%, P = 0.001), whereas stroke volume was not significantly changed (68.4 +/- 22.3 cm3 to 69.1 +/- 22.3 cm3, P = NS) during sinus rhythm at follow-up. In 14 of those patients, discontinuation of pacing resulted in a significant increase of left atrial fractional shortening (8.1% +/- 1.7% to 20.1% +/- 4.3%, P < 0.001) and significant increase of left atrial diastolic dimension compared with paced and preimplantation levels (3.8 +/- 0.7 cm vs 3.6 +/- 0.7 cm and 3.0 +/- 0.5 cm, respectively, P < 0.001). Long-term VVI pacing in patients with sick sinus syndrome results in increase of the left ventricular end-systolic dimension and permanent reduction of the left ventricular ejection fraction. In the left atrium, VVI pacing causes an immediate reduction of the fractional shortening as well as long-term increase of the diastolic dimension.

Aged↗

Radionuclide evaluation of postextrasystolic potentiation of left ventricular function induced by atrial and ventricular stimulation.

Postextrasystolic potentiation of left ventricular function induced by ventricular and atrial stimulation was compared in 10 patients using radionuclide ventriculography. After insertion of pacing wires, a preliminary radionuclide ventriculogram was obtained and then ventricular and atrial trigeminy was induced in random order, each with identical R-R coupling intervals, each for 6 to 10 minutes. During the stimulation studies, radionuclide data were acquired in electrocardiographic gated list mode format. Left ventricular ejection fraction and relative end-diastolic and end-systolic volume changes were measured for each reformatted composite sinus, atrial and ventricular premature beat and potentiated beat. The volume changes were normalized to the count-based values obtained for the sinus beat of the appropriate study. Postextrasystolic potentiation induced by either ventricular or atrial stimulation was characterized by similar significant increases in left ventricular ejection fraction (mean +/- standard deviation 7 +/- 3 percent, p less than 0.01 versus 7 +/- 5 percent, p less than 0.01; difference not significant [NS]) and decreases in relative end-systolic volume (-12 +/- 12 percent, p less than 0.01 versus -12 +/- 8 percent, p less than 0.01; NS) but little change in relative end-diastolic volume (+5 +/- 10 percent, NS versus +4 +/- 7 percent, NS; NS). This was despite a longer compensatory pause (1,120 +/- 220 versus 1,050 +/- 190 ms, p less than 0.01) after the ventricular premature beat. It is concluded that there is no difference in the postextrasystolic potentiation induced by atrial or ventricular premature stimulation.

Adult↗

Measurement of left atrial systolic time intervals in hypertensive patients using Doppler echocardiography: relation to fourth heart sound and left ventricular wall thickness.

The concept of left atrial systolic time intervals and Doppler echocardiography were used in a quantitative assessment of left atrial function in relation to the presence or absence of a fourth heart sound and to left ventricular hypertrophy in 47 patients with hypertension. Left atrial systolic time interval indexes included atrial pre-ejection period (the time between the onset of an electrocardiographic P wave and the onset of left ventricular inflow during atrial systole [A wave]), corrected atrial pre-ejection period (the atrial pre-ejection period divided by the duration of the P wave), and atrial ejection time (the time between the onset and cessation of the A wave). Twenty-one patients with a fourth heart sound on the phonocardiogram had a shorter atrial pre-ejection period (81 +/- 10 versus 89 +/- 14 ms p less than 0.05) and a corrected atrial pre-ejection period (66 +/- 17 versus 83 +/- 18 ms, p less than 0.01), as well as a longer atrial ejection time (147 +/- 15 versus 126 +/- 13 ms, p less than 0.001) than did 26 patients without a fourth heart sound. The ratio of atrial pre-ejection period to atrial ejection time and that of corrected atrial pre-ejection period to atrial ejection time was smaller in patients with than in patients without a fourth heart sound (0.56 +/- 0.08 versus 0.71 +/- 0.11, p less than 0.001; 0.46 +/- 0.16 ms-1 versus 0.67 +/- 0.17 ms-1, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Attenuated nodal response. Apropos of 30 cases].

In a population of 600 consecutive patients undergoing endocavitary electrophysiological study to assess nodal conduction, 40 had an atriohisian Wenckenbach point of over 200/mn. In 30 cases, vagal stimulation with ATP (10 to 40 mg IV) provoked an increase in atrioventricular conduction, with lengthening the AH interval by over 100 p. 100 or transient atrioventricular block. This increase allowed elimination of an accessory atriohisian pathway which could give similar high Wenckenbach points, but which do not show decremental conduction. In all our cases, the conduction passed through the artrioventricular node (AVN) whose response to rapid atrial stimulation was attenuated compared to normal. The parameter of this attenuated nodal response varied from case to case, but in general, the intervals were shorter than normal. The AH interval was less than 50 ms in 22 cases (N = 70 +/- 20 ms). The effective nodal refractory period was shorter than the functional atrial refractory period in 20 cases. The shortest atrial cycles transmitted 1/1 to the ventricles ranged from 230 to 300 ms (274 +/- 33 ms) (N = 375 +/- 40 ms). The functional structure of the AVN was studied by the lengthening of the AH interval with heart rate : 5 types were distinguished : 10 patients had progressive lengthening of AH interval greater than 100 ms (Type I) as in a normal AVN; 5 had progressive lengthening of AH interval of less than 50 ms (Type II), 5 had progressive lengthening of AH which then remained stable for a number of heart rates before lengthening again (Type III); 3 had an initial moderate lengthening of the AH interval which then became more rapid (Type IV) and 7 had no change in AH until 120/mn and then a progressive lengthening was observed (Type V). Two functional groups could also be identified depending on whether the lengthening was progressive, suggesting a single nodal pathway (Types I and II) or on whether differing increases were observed related to the atrial rate, suggesting two (Types IV and V) or even three (Type III) atrionodal or intranodal pathways with different refractory periods. Of these 30 patients, only 14 had documented supraventricular tachycardia, 13 being atrial fibrillation and the other a junctional tachycardia. Attenuated nodal behavior does not seem to be a direct cause of supraventricular arrhythmias but these arrhythmias were not tolerated as well because of the special properties of the atrioventricular node.

Adenosine Triphosphate↗

Left ventricular diastolic function in the normal and diseased heart. Perspectives for the anesthesiologist (1).

Attempts to quantitatively describe ventricular function during diastole have been stimulated by the recognition that diastolic mechanics significantly influence overall cardiac performance, and that diastolic dysfunction may precede, or substantially contribute to, abnormalities of systolic function in various pathologic conditions (table 1). Indices of diastolic function can be derived invasively or noninvasively, and focus on the measurement of a diverse and complex set of separate, but intimately interrelated, processes that, while complementary, may not be directly comparable. Measurement of these indices is complicated, because diastolic function depends on several determinants: active, energy-dependent forces (isovolumic ventricular relaxation); passive and dynamic filling characteristics (chamber and myocardial stiffness); and extrinsic factors (left atrial function, ventricular interaction, valvular integrity, pericardial restraint, and myocardial blood flow), as well as other conditions that affect myocardial function during systole (preload, afterload, heart rate, and inotropic state). The diversity of events occurring during diastole indicates that a single index of diastolic function cannot adequately describe this period of the cardiac cycle, and the physiologic implications of diastolic dysfunction may be different, depending on the period of diastole affected (table 1). Thus, assessment of diastolic function is complicated, because of the heterogeneity of the event and the multiple factors that influence it. Despite the inherent potential limitations of indices describing diastolic function, these parameters provide useful references for evaluating the natural history of patients with diastolic heart failure, for assessing the benefits of therapeutic interventions of anesthetic actions, and for enhancing our knowledge of cardiac pathophysiology.

Anesthesiology↗

Atrial form and function: lessons from human molecular genetics.

Molecular genetic analyses of human hereditary disorders that affect cardiac atrial structure and function have recently identified several genes that regulate atrial morphogenesis. Mutations of the TBX5, NKX2.5, EVC, and PRKAR1 alpha genes all result in abnormalities of human atrial growth and development, and mutations in at least one gene results in familial atrial fibrillation and is as yet unidentified. Ongoing studies to find interactions between these transcription factors and intracellular signaling molecules and other as yet unknown genes are establishing critical pathways in human cardiogenesis. Human investigation and experimental animal models of heart development synergize to elucidate etiologies of common congenital heart disease.

Abnormalities, Multiple↗

Species-dependent effects of increasing hypoxia on functions and energy balance in isolated atria.

1. The hypoxia-induced changes of contractile force, frequency and diastolic tension in isolated atria from guinea pig, rat and rabbit were studied together with tissue content of adenine nucleotides, creatine phosphate and lactic acid. 2. Increasing hypoxia induced a progressive reduction of contractility in guinea pig, rat and rabbit atria. Hypoxia also induced a progressive reduction of frequency in rat atria, whereas atrial rate decreased significantly only during drastic hypoxia in guinea pig and rabbit. In spontaneously beating atria, hypoxia increased diastolic tension only in rat. 3. After 30 min of drastic hypoxia, ATP decreased in guinea pig and rabbit but not in rat atria. Creatine phosphate decreased and lactic acid increased in all three species. 4. These data suggest that: (a) hypoxia-induced changes in atrial function and in metabolic content are species-dependent; (b) hypoxia-induced inhibition of atrial activity could represent protection aimed at saving energy.

Animals↗

Changes in atrioventricular conduction properties with refractory-period modulation.

Dofetilide, clofilium, and risotilide, three drugs known to prolong cardiac action potentials and refractory periods, were studied by using a perfused isolated rabbit heart preparation with intermittent premature pacing and bipolar surface electrograms. The rate-related effects of these drugs on atrioventricular (AV) conduction were tested by pacing at a long (400 ms) and a short (250 ms) basic cycle length (BCL). All three drugs increased refractory periods in a concentration-dependent manner in most segments of the AV axis. The maximal atrio-His (AH) conduction interval (AHmax) and delta AH (AHmax - AHmin) produced by premature pacing was decreased by the highest concentration of each drug at the 400-ms BCL, whereas only clofilium reduced AHmax and delta AH at the 250-ms BCL. Changes in delta AH correlated best with changes in the atrial functional refractory period. The His-Purkinje system conduction interval (HV), represented by delta HV, was unaffected by any drug at either BCL. These results show that if atrial or nodal refractory periods are increased sufficiently, AHmax but not AHmin was decreased at the 400-ms BCL. Because dofetilide and risotilide did not affect AHmax at the 250-ms BCL, these drugs may be less effective at preventing AV nodal reentrant tachycardias than a drug such as clofilium that displays less rate dependency.

Animals↗

Atrial fibrillation in hypertrophic cardiomyopathy: mechanisms, embolic risk and prognosis.

Hypertrophic cardiomyopathy (HCM) is associated with an increased incidence of supraventricular and ventricular arrhythmias. Atrial fibrillation (AF) is the most common arrhythmia in HCM with a prevalence of 20% and an annual incidence of two percent per year. Increased left atrial size and volume along with impaired left atrial function confer an increased likelihood of AF. The onset of AF is often accompanied by a decrease in functional status in conjunction with an increased risk of stroke and overall mortality.

Atrial Fibrillation↗

Usefulness of B-type natriuretic peptide in hypertensive patients with exertional dyspnea and normal left ventricular ejection fraction and correlation with new echocardiographic indexes of systolic and diastolic function.

B-type natriuretic peptide (BNP) levels increase in systolic heart failure (HF). However, the value of BNP in hypertensive patients with suspected diastolic HF (symptoms suggestive of HF but normal ejection fraction) and its relation to myocardial function in these patients is unclear. We prospectively studied 72 ambulatory hypertensive subjects (40 women, mean age 58 +/- 8 years) with exertional dyspnea and ejection fraction > or =50%. Diastolic function was evaluated with transmitral and pulmonary venous Doppler, mitral annular velocities (pulsed-wave tissue Doppler), and flow propagation velocity (color M-mode). Systolic function was assessed with strain and strain rate derived from color tissue Doppler imaging. BNP was related to myocardial function and the presence or absence of global diastolic dysfunction. By conventional Doppler criteria, 34 patients had normal left ventricular diastolic function and 38 had isolated diastolic dysfunction. BNP values were higher in patients with diastolic dysfunction (46 +/- 48 vs 20 +/- 20 pg/ml, p=0.004) and were related independently to blood pressure, systolic strain rate, left atrial function (p<0.01 for all), and age (p=0.015). Patients with diastolic dysfunction and pseudonormal filling had higher BNP levels compared with impaired relaxation (89 +/- 47 vs 35 +/- 42 pg/ml, p=0.001). However, 79% of patients with diastolic dysfunction had BNP levels within the normal range. We conclude that in ambulatory hypertensive patients with symptoms suggestive of mild HF and normal ejection fraction, BNP is related to atrial and ventricular systolic parameters, blood pressure, and age. Although elevated in the presence of diastolic dysfunction, the BNP level mostly is in the normal range and, therefore, has limited diagnostic value in stable patients with suspected diastolic HF.

Biomarkers↗