Superior left atrial approach to the mitral valve: incidence of postoperative arrhythmia.

BACKGROUND AND AIM OF THE STUDY: The superior left atrial approach to mitral surgery involves exposure of the mitral valve through a longitudinal, craniocaudally orientated incision in the roof of the left atrium. The study aim was to evaluate the incidence of postoperative arrhythmias following this procedure. METHODS: Fifty-nine patients underwent either mitral valve repair (n = 20), mitral valve replacement (n = 26) or an associated procedure (n = 13), including aortic valve replacement, coronary artery bypass grafting and atrial septal defect closure. Eight patients had undergone previous surgery on the mitral valve. Patients were classified according to their preoperative rhythm: sinus rhythm (SR), paroxysmal or chronic atrial fibrillation (AF), or permanent pacing. Changes in cardiac rhythm were evaluated postoperatively, after four weeks, and at late follow up (mean 23.8 months). RESULTS: Preoperatively, 24 patients had shown SR, 10 had paroxysmal AF, 24 had chronic AF, and one patient had permanent pacing. At the time of discharge, SR was recorded in 18 patients who had SR preoperatively, in seven who had paroxysmal AF preoperatively, and in one patient who had chronic AF preoperatively. At follow up, SR was seen in 19 patients with preoperative SR, in seven with paroxysmal AF preoperatively, and in two with chronic AF preoperatively. Four patients received permanent pacemakers postoperatively due to total heart block or bradycardia. CONCLUSION: The superior left atrial approach to mitral valve surgery appears to be safe as it maintains the sinus rhythm in a high proportion of patients postoperatively. In addition, it is not normally prone to technical complications.

If in left human atrium: a potential contributor to atrial ectopy.

OBJECTIVE: The left human atrium plays an important role in initiation of atrial fibrillation (AF) and the hyperpolarization activated cation current (I(f)) is a candidate for contributing to abnormal automaticity. However, electrophysiological data concerning I(f) are not available in this cardiac region and we therefore investigated I(f) in human left atrial tissue. METHODS: Human atrial myocytes were isolated from the left atrial appendage (LAA) and the left atrial wall (LAW) obtained from patients undergoing open heart surgery. I(f) was measured with the whole-cell patch-clamp technique. RESULTS: I(f) densities between -70 and -110 mV were found to be significantly higher in LAA than in LAW cells. Furthermore, in the group of LAA cells the half maximal activation potential (V(1/2)) was found to be less negative (V(1/2) of -84.3+/-1.9 mV, n=14/9) compared to LAW cells (V(1/2) of -97.8+/-2.1 mV, n=28/9). Beta-adrenergic receptor stimulation with isoproterenol (1 microM) caused an acceleration of current activation and a V(1/2) shift to more positive potentials in cells of both regions (LAA: 8.8+/-2.3 mV, n=6/4 and LAW: 8.9+/-2.6 mV, n=6/4). Simulations using a mathematical model of the human atrial myocyte demonstrated that I(f) was able to induce spontaneous activity in the model at a regular rhythm due to the interplay of I(f), Na(+)/Ca(2+) exchange current and Ca(2+) release of the sarcoplasmic reticulum (SR). CONCLUSIONS: Our study revealed the presence of I(f) in left atrial myocytes and showed that I(f) parameters depend on atrial region. I(f) current densities were sufficient to convert the mathematical model of a quiescent human atrial cell into a "pacemaker cell". These data support the hypothesis of I(f) as a contributor to abnormal automaticity in human atrial tissue.

Hyperhomocyst(e)inemia and Chlamydia pneumoniae IgG seropositivity in patients with coronary artery disease.

Elevated levels of homocyst(e)ine and infection by Chlamydia pneumoniae have been hypothesized individually to play a role in coronary artery disease (CAD), but the mechanisms are unclear. Data on a possible association are not available. We investigated the correlation between IgG antibody titers against C. pneumoniae and fasting plasma homocyst(e)ine in 234 consecutive male patients with CAD. Chlamydial antibodies to a recombinant genus-specific lipopolysaccharide (LPS) were measured with ELISA. Total homocyst(e)ine (tHcy) concentrations were measured by high-performance liquid chromatography (HPLC). Thirty-seven subjects were classified hyperhomocyst(e)inemic (fasting homocyst(e)ine>14 micromol/l, group A), and 197 subjects were below cut-off (tHcy<14 micromol/l, group B). Prevalence of IgG seropositivity against C. pneumoniae was significantly higher in group A (68%) as compared to group B (39%, P=0.002). Antibody titers were also significantly higher in hyperhomocyst(e)inemic subjects than in cases with low homocyst(e)ine levels (P=0.002). Overall titers correlated significantly with tHcy levels (r(2)=0.222, P=0.001). Hyperhomocyst(e)inemia was associated with arterial hypertension (P=0.003), intake of lipid lowering drugs (P=0.022) and quite not with low folate concentration (P=0.052). No association was seen for IgG seropositivity or homocyst(e)ine and age, body mass index, smoking, diabetes, vitamin B(6) and B(12), cholesterol and triglycerides. These data indicate an association between elevated plasma homocyst(e)ine concentrations and chlamydial IgG antibody titers in patients with CAD.

Angiotensin-converting enzyme polymorphisms and their potential impact on left ventricular myocardial geometry after aortic valve surgery.

BACKGROUND AND AIM OF THE STUDY: Genetic variants of the angiotensin-converting enzyme (ACE) cascade may influence left ventricular myocardial mass (LVMM) regression after aortic valve surgery. Postoperative long-term changes in LV indices were investigated in patients with asymptomatic aortic regurgitation (AR) and symptomatic aortic stenosis (AS) and related to alleles of ACE polymorphisms. METHODS: A total of 96 patients was included in the study, 21 with class IIa AR (22%) and 75 with class I AS (78%) recommendations for surgery. Patients were evaluated for demographic risk factors and underwent a thorough clinical examination including 3-D cardiac imaging by ultrafast-computed tomography. Genomic DNA was isolated for genotyping. RESULTS: AR patients were younger (55.8 +/- 8.9 versus 64 +/- 9.1 years, p = 0.0014), had a larger body surface area (1.92 +/- 0.21 versus 1.82 +/- 0.19 m2, p = 0.039), and were more likely to be asymptomatic (myocardial infarction, p = 0.04; syncope, p = 0.0099; thromboembolism, p = 0.03; NYHA class IV, p = 0.04). Postoperatively, the reduction in absolute LVMM (from 297.1 +/- 52.6 to 190.1 +/- 57.1 g versus 214.4 +/- 55.7 to 143.8 +/- 40.0 g; pT = 0.0000001) and indexed LVMM (from 156.0 +/- 31.7 to 99.3 +/- 28.4 g/m2 versus 118.7 +/- 28.3 to 79.3 +/- 20.6 g/m; pT = 0.0000001) over time was more significant in AR patients, but never reached normal values. Enforced ACE inhibitor medication resulted in significantly higher postoperative indexed LVMM differences in homozygote DD patients compared to AR patients with II/ID alleles of ACE 16 ins/del polymorphism. CONCLUSION: AR patients showed a statistically significant decrease in absolute/indexed LVMM during follow up, but never achieved LV mass recovery compared to standard values or to values in patients undergoing aortic valve replacement for AS. The benefits of ACE inhibitors were observed among AR patients with homozygote DD alleles of ACE 16 ins/del polymorphism.

Late dissection of the ascending aorta after previous cardiac surgery: risk, presentation and outcome.

OBJECTIVE: Aortic dissection is a potentially life-threatening condition and may follow surgical interventions as a complication with distinct presentation and high mortality. Information on the incidence and etiology of aortic dissections following cardiac surgery is sparse and inconsistent. The true incidence of this entity may so far have been underestimated. METHODS: Data of 223 operations on the thoracic aorta performed exclusively at our institution between January 1990 and May 2001 were analysed for clinical and prognostic features. Patients with Marfan syndrome and traumatic cases were not included. Cases of type A aortic dissection following cardiac surgery were investigated further. RESULTS: Dissection of the ascending aorta occurred in 83 patients, of whom 11 (13.2%, six acute and five chronic) had undergone previous cardiac surgery (four aortic valve replacements (AVR), two double valve replacements (DVR), two AVR+coronary artery bypass grafts (CABG), three CABGs). The time interval between first operation and dissection was 0.2-17 years (median 3.3 years). Eight (72%) patients had arterial hypertension. The aortic diameter was >or=50mm in all 11 cases upon presentation. Dissections were treated with Bentall procedures (3), Cabrol procedure (1), supracoronary tube graft (6) including concomitant CABG (3) and AVR with local repair (1). Total in-hospital mortality was 54% (6/11), and 66% (4/6) in cases with acute dissection due to low cardiac output (3) and myocardial infarction (3). CONCLUSIONS: Type-A aortic dissection can follow cardiac operations at any time with no typical interval or associated histology and with high overall hospital mortality. Male patients with arterial hypertension are at increased risk. Clinical presentation may differ from primary dissection with implications for management and risk estimation.

Forty-one-month follow-up of the Symmetry aortic connector system for proximal venous anastomosis.

OBJECTIVE: Results of short- and midterm follow-up studies of the patency rate of the Symmetry aortic connector systems (St Jude Medical, Inc, Minneapolis, Minn) are controversial. Long-term follow-up studies are still lacking (so far, the longest mean follow-up period was 19 months). The aim of our study was (1) to evaluate the patency rate of this device over a longer time-period and (2) to analyze risk factors for graft occlusion. METHODS: Between November 2000 and July 2003, 76 Symmetry aortic connector systems were implanted in 42 patients. At follow-up, 24 patients with 44 mechanical connectors were studied with 64-slice cardiac computed tomography. Eight patients had died previously, 6 patients refused to undergo a computed tomographic scan, and 4 patients had to be excluded because of impaired renal function. RESULTS: From a total of 44 mechanical connectors studied, 24 (55%) were occluded, 20 (45%; confidence intervals 31%-61%) were patent, and 7 of these grafts showed stenosis in the area of the connector. Mean follow-up was 41 +/- 10 months (18-52 months). Sex, age, left main stenosis, hyperlipidemia, hypertension, renal failure, target vessel, stenosis of the target vessel, diameter of the target vessel, type of surgical intervention, diabetes, ejection fraction, postoperative anticoagulation regimen, and the connector size showed no significant influence on the bypass graft patency (P > .05). The bypass graft flow was recognized to be the only risk factor for bypass graft occlusion (P = .0256). CONCLUSION: Midterm follow-up data show a high number of occluded Symmetry aortic connector system vein grafts. On the basis of these observations, the use of the connector was abandoned at our institution.

A hyperpolarization activated inward current (If) is present in infant ventricular myocytes.

I(f) was shown to be present in adult human atrial and ventricular myocytes but data obtained from infant myocytes are lacking. We have studied I(f) in isolated ventricular myocytes from children undergoing surgical correction of tetralogy of Fallot (TOF; n = 5; mean age: 15.3 months). All recordings were made with the patch clamp technique in the whole cell mode at a temperature of 36-37 degrees C. A modified Tyrode solution containing 25 mM KCl was used to amplify I(f). Considering I(f) to be present when its current density at -120 mV was greater than 0.5 pA/pF, I(f) could be found in 28 out of 32 myocytes (88%). The mean current density was -2.01 +/- 0.3 pA/pF (mean +/- S.E.M.). First current activation occurred at -70 mV and I(f) could be reversibly inhibited by superfusing the myocytes with CsCl (2 mM). Half maximal activation (V(1/2)) of I(f) was at -80.3 +/- 1.0 mV (n = 28). Beta-adrenergic receptor stimulation with isoproterenol (1 microM) caused an acceleration of current activation and a shift of V(1/2) by 7.88 +/- 1.8 mV (n = 10) to less negative potentials. This study provides first evidence that the hyperpolarization-activated pacemaker current I(f) is present in infant human ventricular myocytes. Our results suggest that I(f) in ventricle of infants suffering from TOF has similar properties as I(f) in adult ventricle.