Early results after mitral valvuloplasty for pure mitral regurgitation

In this study we present the results of 105 consecutive patientswith pure mitral regurgitation who underwent surgical treatment.In all patients mitral regurgitation was associated with mitralvalve prolapse: 54 patients underwent mitral valvuloplasty and51 patients mitral valve replacement. Clinical assessment and echocardiography were used as follow-upcriteria at one year after surgery. After mitral valvuloplasty,NYH A decreased from 2.7±0.8 to 1.1±0.7 (P<0.01)and workload capacity increased from 65±28% to 96±25%(P<0.001); left endsystolic atrial dimension and enddiastolicdimension decreased from 6.2±0.8 to 4.8±1.2 cm(P<0.001) and from 7.2±1.3 to 5.9±0.8 cm (P<0.01);ventricular contraction fraction did not change significantly. After mitral valve replacement, clinical and echocardiographicimprovement was significant but less remarkable than after valvuloplasty;ventricular contraction fraction fell from 39±7% to 29±8%in contrast to patients undergoing mitral valvuloplasty in whomno significant change occurred. Complications were rare in both groups though only a minorityof patients undergoing mitral valvuloplasty received anticoagulants.We conclude that mitral valvuloplasty in patients with puremitral regurgitation associated with mitral valve prolapse givesexcellent results, particularly regarding left ventricular functionwhen compared with the patients after mitral valve replacement.     

Detection of virulence genes of Clostridium difficile by multiplex PCR

Antikainen J, Pasanen T, Mero S, Tarkka E, Kirveskari J, Kotila S, Mentula S, Könönen E, Virolainen‐Julkunen A‐R, Vaara M, Tissari P. Detection of virulence genes of Clostridium difficile by multiplex PCR. APMIS 2009; 117: 607–13. Clostridium difficile strains belonging to the PCR ribotype 027, pulse‐field gel electrophoresis (PFGE) type NAP1, toxinotype III and restriction endonuclease analysis group BI harbouring mutations in the tcdC gene and possessing binary toxin components A and B have been described to cause epidemics with increased morbidity and mortality. In the present study we developed a conventional multiplex PCR designed to detect selected virulence associated markers of the hypervirulent C. difficile PCR ribotype 027. The multiplex PCR assay detected the major toxins A and B, binary toxin components A and B as well as a possible deletion in the tcdC gene: a characteristic pattern of amplification products for the PCR ribotype 027 strains was detected. This rather simple method was specific for the screening of this hypervirulent C. difficile strain. The correlation between the multiplex PCR and PCR ribotyping methods was excellent. The sensitivity and specificity were 100% in our epidemiological situation. In conclusion, this multiplex PCR was found useful in the preliminary screening for the hypervirulent C. difficile PCR ribotype 027.     

The Asn-291→Ser and Ser-477→Stop mutations of the lipoprotein lipase gene and their significance for lipid metabolism in patients with hypertriglyceridaemia

We examined 99 Finnish patients whose serum fasting triglycerides (TG) had exceeded 6.0 mmol L^?1, with special interest to their lipid, lipoprotein and post-heparin plasma lipase activities. The control group consisted of 75 healthy individuals. We also determined the frequency of the Asn-291→Ser and Ser-447→Stop mutations both in hypertriglyceridaemic (HTG) subjects and in control subjects. A total of 51 of the original 99 hypertriglyceridaemic patients still had TG > 6.0 mmol L^?1 when measured a second time. They are referred to as persistently hypertriglyceridaemic subjects (pHTG). The remaining 48 subjects had TG < 6.0 mmol L^?1 in the second measurement and are referred to as sporadically hypertriglyceridaemic subjects (sHTG). The allelic frequencies of the Ser-447→Stop mutation in the total HTG and sHTG groups were similar to the frequencies present in the control group, but lower in pHTG patients compared with the control group (0.049 vs. 0.153, χ² = 6.63, P < 0.05). The Asn-291→Ser mutation was more frequent in HTG group than in the control group (0.0606 vs. 0.013, χ² = 4.86, P < 0.05). This difference was due to the higher frequency of the minor allele of Asn-291→Ser in the cohort with persistent hypertriglyceridaemia compared with the control group (0.088 vs. 0.013, χ² = 8.00, P < 0.01 ). The highest frequency (0.114) of the minor allele of Asn-291→Ser was found in type 2 diabetic patients with persistent hypertriglyceridaemia. The carrier status of Asn-291→Ser or Ser-447→Stop did not predict either post-heparin plasma lipoprotein lipase (LPL) activities or lipid and lipoprotein levels in any of the groups studied. Our data suggest that overproduction of very low-density lipoproteins (VLDL) is a more important cause of hypertriglyceridaemia in the Finns than is the LPL deficiency.     

Early results after mitral valvuloplasty for pure mitral regurgitation

In this study we present the results of 105 consecutive patientswith pure mitral regurgitation who underwent surgical treatment.In all patients mitral regurgitation was associated with mitralvalve prolapse: 54 patients underwent mitral valvuloplasty and51 patients mitral valve replacement. Clinical assessment and echocardiography were used as follow-upcriteria at one year after surgery. After mitral valvuloplasty,NYH A decreased from 2.7±0.8 to 1.1±0.7 (P<0.01)and workload capacity increased from 65±28% to 96±25%(P<0.001); left endsystolic atrial dimension and enddiastolicdimension decreased from 6.2±0.8 to 4.8±1.2 cm(P<0.001) and from 7.2±1.3 to 5.9±0.8 cm (P<0.01);ventricular contraction fraction did not change significantly. After mitral valve replacement, clinical and echocardiographicimprovement was significant but less remarkable than after valvuloplasty;ventricular contraction fraction fell from 39±7% to 29±8%in contrast to patients undergoing mitral valvuloplasty in whomno significant change occurred. Complications were rare in both groups though only a minorityof patients undergoing mitral valvuloplasty received anticoagulants.We conclude that mitral valvuloplasty in patients with puremitral regurgitation associated with mitral valve prolapse givesexcellent results, particularly regarding left ventricular functionwhen compared with the patients after mitral valve replacement.     

Predictability of aortic dissection as a function of aortic diameter

The role of aortic diameter on the occurrence of type A dissectionwas investigated in 73 patients with dilated ascending aortaat the lime of pre-operative evaluation. Using transthoracicechocardiography for diagnosis and measurements, 54 patientswere identified with type A dissection (group 1) and 19 withoutdissection (group 2). The true mean aortic diameters were identical(6·0±1·3 cm in group 1 and 6·4±1·4cm in group 2; mean±SD; ns) as were the indexed aorticdiameters (ratio of diameter/body surface area; 3·2±0·8cm . m^–12 and 3·4±0·7cm m^–2respectively; ns). However, the individual diameters showeda pronounced scatter in both groups (range from 3·6±11·0cm). Of the 73 patients, 66 had surgery (47/54 with and 19/19without dissection) and seven patients were treated medically.Emergency surgery was performed in 45/66 patients (all withacute type A dissection) andelective repair in 21/66 (19 withoutand two with chronic type A dissection). In-hospital mortalitywas 18% in the emergency group, 5% in the elective group and57% in the medical group. It is concluded that patients with dilated ascending aorta havea substantial incidence of acute dissection. Their clinicalcourse is unpredictable; acute dissection occurs in some, andin others the ascending aorta continues to enlarge without dissection.Because patients with dissection often arrive too late for electiverepair andhave to be operated on as emergencies with a higheroperative risk, we recommend elective surgery before the diameterof the ascending aorta has reached 6 cm.     

Dynamics of aortic flow in hypertrophic cardiomyopathy

The purpose of this study was to reassess left ventricular ejectiondynamics in hypertrophic cardiomyopathy, to investigate whethera premature stoppage of ejection occurs, as previously reported,and whether reliable criteria for left ventricular outflow tractobstruction can be established by non-invasive evaluation ofaortic flow patterns. In a group of 21 patients with hypertrophiccardiomyopathy, composed of 9 with the obstructive form (HOCM),9 with the non-obstructive form (HNCM) and 3 with apical hypertrophy(HACM), instantaneous flow velocities across the ascending aortawere determined non-invasively with a 16-gated Doppler 2-D echoinstrument. Ten normals served as controls. The 16 flow velocitieswere averaged over 8 heart beats and the relative volume flowrate was calculated by microprocessor analysis. Ejection time(i.e. flow time) derived from the flow curves was compared withthe available ejection period as determined from the carotidpulse tracing. In normals, ejection time amounted to 94±3%of the available ejection period, in HOCM to 92±5% andin HNCM to 93±4% (no significant differences). In HACM,however, ejection time was reduced to 71±14% of the availableejection period. In contrast to HNCM, aortic flow in HOCM wascharacterized by an early peak followed by a plateau at a sizeablylower flow level for the rest of systole. Flow time of an abnormallyshort duration was the hallmark of HACM. We conclude that inpatients with hypertrophic cardiomyopathy, HOCM and HNCM canbe distinguished by the shape of their volume flow curves. Apremature stoppage of ejection is only found in patients withHACM.     

Left ventricular flow from apex to base during systole and isovolumic relaxation in a patient with hypertrophic cardiomyopathy and midventricular obstruction

The occurrence of a left ventricular anterograde flow velocity(maximal: 3·9m . s^–1) is demonstrated in a 32-year-oldpatient with hypertrophic cardioinyopathy and midveniricularobstruction, beginning at early systole and persisting throughoutthe isovolumic relaxation. Cardiac catheterization with simultaneousdual high fidelity pressure measurements in the apical and basalchambers confirmed the presence of the Doppler maximal instantaneouspressure gradient of 60 mmHg. Contrast left ventricular angiographyexcluded apical dyskinesia. In the two intracavity compartments,isovolumic relaxation time and the time constant of pressuredecay () were abnormal whereby was more delayed in the apicalthan in the basal portion. The presence of an apical high pressurezone during systole with impeded and delayed emptying throughthe midventricular obstacle and the late onset and prolongationof relaxation are thought to be the cause of the intraventricularflow from apex to base lasting from early systole throughoutisovolumic relaxation.