LAW No. 167 of 16 JULY 1997 OF THE REPUBLIC OF KAZAKHSTAN THE CRIMINAL CODE OF THE REPUBLIC OF KAZAKHSTAN 4 page

The development of increased ventricular mass and its regression after reparative surgery are important properties of ventricular myocardium.190–192 An increase in ventricular mass in excess of the normal process of growth is determined by the nature of the inciting stimulus (hemodynamic or hypoxic), the duration and type of the hemodynamic stimulus (pressure or volume overload), myocardial age (maturity) at the time the stimulus is imposed, and the cell type that is involved.191–193 The response of a given cell type to a hemodynamic or hypoxic stimulus depends chiefly upon myocyte maturity. If overload or hypoxia is imposed on the immature heart, the cellular response is characterized by replication (hyperplasia) of myocytes and fibroblasts.194 If the stimulus continues beyond immaturity, myocytes respond by hypertrophy (enlargement) and fibroblasts by hyperplasia (replication).192 An unresolved concern is the cellular basis for the regression in mass after surgical relief from ventricular overload or hypoxia (Fig. 30–18 Fig. 30–18 ). The fate of myocytes that replicate in excess of their genetically regulated numbers has not been established.195 A postoperative reduction in ventricular mass in the setting of hyperplasia implies, at least in part, that the numerically excessive myocytes become smaller in size, not fewer in number. If this contention is valid, its long-term functional significance is unknown. The response of connective tissue cell hyperplasia to operative removal of the overload or hypoxic stimulus is also unknown, although there is evidence that connective tissue cells do not regress as readily as myocytes.196

VASCULAR RESIDUA

VASCULAR RESIDUA. Vascular residua consist of anatomical anomalies or defects or elevated resistance and/or pressure in the systemic or pulmonary circulation. Examples include the relationship between aortic root disease and bicuspid aortic valve and rupture of an aneurysm of the circle of Willis associated with coarctation of the aorta.

Congenital anomalies of the coronary arteries coexist with a number of congenital malformations of the heart.5 Examples include Fallot’s tetralogy and the residual coronary artery disease (intimal proliferation, medial thickening, premature atherosclerosis) initiated by the hypertension of coarctation of the aorta. The preoperative status of the pulmonary vascular bed, especially the resistance vessels, is a major determinant of the presence and degree of residual postoperative pulmonary vascular disease. Refinements and improved safety that currently permit surgical repairs within the first 6 to 12 months of life make it likely that postoperative pulmonary vascular disease will become less and less a postoperative residuum.

NONCARDIOVASCULAR RESIDUA

NONCARDIOVASCULAR RESIDUA. These can be important long-term concerns after reparative surgery.189 Developmental abnormalities such as the mental retardation of Down syndrome or the physical abnormalities of Turner’s or the Ellis-van Creveld syndrome are examples. Residual somatic defects include dysmorphism and limb abnormalities. Psychosocial disorders may exist as important postoperative residua, and a healed brain abscess can serve as a focus of a seizure disorder. Cataracts and deafness persist as residua after division of the patent ductus in children with the rubella syndrome.

Sequelae

Sequelae

Sequelae relate to electrophysiological disturbances, native cardiac valves, prosthetic materials, myocardium, and endocardium (Table 30–4 Table 30–4 ). Electrophysiological sequelae after intraatrial repair are represented by disturbances in rhythm and conduction, sinoatrial dysfunction, junctional rhythm, atrial fibrillation, atrial flutter, and impaired atrioventricular conduction varying from prolongation of the P-R interval to complete atrioventricular block. Electrophysiological sequelae after intraventricular repair through a right atrial incision result from injury to internodal pathways and to the proximal right bundle branch alone or in combination with the left anterior fascicle.197 A right ventriculotomy is responsible for two electrophysiological sequelae: an alteration in the sequence of ventricular activation and electrical instability of the incised right ventricle. The surface ECG is useful in determining the proximal origin of abnormal right ventricular activation when right bundle branch block coexists with left anterior fascicular block.197 Bifascicular block sets the stage for postoperative complete heart block, which is an uncommon but hazardous electrophysiological sequel (Fig. 30–17 Fig. 30–17 ).

Sequelae involving native cardiac valves occur after left ventricular or right ventricular outflow repairs, or left ventricular or right ventricular inflow repairs. Postoperative aortic regurgitation as a sequel of surgery for congenital bicuspid aortic stenosis is an example. Surgical repair or balloon dilatation of congenital pulmonary valve stenosis is often followed by mild pulmonary regurgitation, a physiologically minor and therefore acceptable sequel. Repair of complex obstruction to right ventricular outflow, as in Fallot’s tetralogy, usually induces pulmonary regurgitation, the importance of which depends on the degree of regurgitant flow and the functional state of the right ventricle.

Sequelae associated with left ventricular inflow repairs accompany operations for congenital mitral regurgitation or congenital obstruction to left ventricular inflow. Assuming complete relief of the mitral regurgitation associated with an atrioventricular septal defect, morphological abnormalities intrinsic to the congenitally malformed valve leave the left ventricular inflow guarded by an abnormal mitral apparatus. Reconstruction of the tricuspid valve in Ebstein’s anomaly is somewhat analogous. Repair is necessarily followed by sequelae intrinsic to the basic tricuspid valve malformation, even if competence is established.

PROSTHETIC MATERIALS

PROSTHETIC MATERIALS. Insertion of these materials represents a special category of sequelae after reparative surgery for congenital heart disease. Certain materials are exceptions, such as an endogenous pericardial patch for closure of an ostium secundum atrial septal defect or a synthetic patch that is entirely covered by a neointimal layer. Valve replacement results in sequelae that vary in significance according to the physical and hemodynamic characteristics of the prosthetic device (bioprosthetic or rigid), the site of insertion, and patient age at the time of operation. Reoperation is required when an infant or child outgrows the original valve prosthesis. Bioprosthetic valves degenerate at rates determined chiefly by patient age at the time of insertion, and by the tissue characteristics of the device (endogenous or exogenous materials, homografts or xenografts). Susceptibility to infective endocarditis varies from negligible with aortic homografts to high with mechanical prostheses. The incidence of thromboembolic complications is low with an aortic homograft and high with a rigid mitral prosthesis. Anticoagulants reduce but do not eliminate thromboembolic complications and carry the inherent risk of anticoagulant-induced bleeding and the risk of teratogenicity during pregnancy.

Conduits can be nonvalved (usually synthetic) or valved (bioprosthetic or mechanical) and pose the risks of degeneration, thrombogenicity, anticoagulation, and infective endocarditis. In addition, conduits—especially valved—are subject to pseudointimal proliferation (peel).2 Conduit obstruction can therefore result from both nongrowth of the device and pseudointimal proliferation.

MYOCARDIAL SEQUELAE

MYOCARDIAL SEQUELAE. Morphological or mechanical sequelae at the site of the ventriculotomy or atriotomy are usually negligible unless there is formation of an aneurysm, which is more properly considered a complication. Electrophysiological sequelae were discussed earlier. Certain endocardial sequelae after intraventricular repair have been called “surgical fibroelastosis.”198,199 The cause and functional significance of these endocardial lesions, which are not necessarily confined to the chamber in which the intracardiac repair was done, have not been established.

REFERENCES

1. Perloff, J. K.: Pediatric congenital cardiac becomes a postoperative adult. The changing population of congenital heart disease. Circulation 47:606, 1973.

2. Perloff, J. K., and Child, J. S.: Congenital Heart Disease in Adults. Philadelphia, W. B. Saunders Company, 1991.

3. Perloff, J. K.: Congenital heart disease in adults: A new cardiovascular subspecialty. Circulation 84:1881, 1991.

4. Perloff, J. K. (Chairman): 22nd Bethesda Conference: Congenital heart disease after childhood: An expanding patient population. J. Am. Coll. Cardiol. 18:311, 1991.

5. Perloff, J. K.: The Clinical Recognition of Congenital Heart Disease. 4th ed. Philadelphia, W. B. Saunders Company, 1994.

6. Fallot, A.: Contribution a l’anatomie pathologique de la maladie bleue (cyanose cardiaque). Marseillemйd. 25:418, 1888.

7. Abbott, M. E.: Atlas of Congenital Heart Disease. New York, The American Heart Association, 1936.

8. Gross, R. E., and Hubbard, J. P.: Surgical ligation of a patent ductus arteriosus: report of first successful case. JAMA 112:729, 1939.

9. Blalock, A., and Taussig, H. B.: Surgical treatment of malformations of the heart in which there is pulmonary stenosis or pulmonary atresia. JAMA 128:189, 1945.

10. Crafoord, C., and Nylin, G.: Congenital coarctation of the aorta and its surgical treatment. J. Thorac. Surg. 14:347, 1945.

11. Kirklin, J. W., DuShane, J. W., Patrick, R. T., et al.: Intracardiac surgery with the aid of a mechanical pump-oxygenator system (Gibbon type): Report of eight cases. Proc. Staff Meet. Mayo Clin. 30:201, 1955.

12. Ritchie, J. L., Cheitlin, M. D., Hlatky, M. A., et al.: Task Force 5: Profile of the cardiovascular specialist: Trends in needs and supply and implications for the future. J. Am. Coll. Cardiol. 24:313, 1994.

13. Roberts, W. C.: The congenitally bicuspid aortic valve: a study of 85 autopsy cases. Am. J. Cardiol. 26:72, 1970.

LAW No. 167 of 16 JULY 1997 OF THE REPUBLIC OF KAZAKHSTAN THE CRIMINAL CODE OF THE REPUBLIC OF KAZAKHSTAN

Latest amendment:

17) Law №10 of 9th December 2004 of the Republic of Kazakhstan. Concerning the Introduction of amendments and additions to the Criminal, Criminal Procedural? Criminal Executive codes of the Republic of Kazakhstan on issues of simplification of procedures for investigation of criminal cases, decriminalization of certain corpora delicti and improvement of the legislation concerning administrative violations.

Section I. Criminal Law

Article 1. Criminal Legislation of the Republic of Kazakhstan

1. The criminal legislation of the Republic of Kazakhstan shall consist exclusively of the present Code of the Republic of Kazakhstan. Other laws which stipulate criminal liability shall only be subject to application after their inclusion into the present Code.

2. The present Code is based on the Constitution of the Republic of Kazakhstan and generally accepted principles and norms of international law.

Article 2. Objectives of the Criminal Code

1. Objectives of the Criminal Code shall be as follows: the protection of the rights, freedoms, and legitimate interests of individuals and of citizens, as well as of property, rights, and legitimate interests of organizations, public order and safety, the environment, constitutional order, and territorial integrity of the Republic of Kazakhstan, the interests of society and the state protected by law from criminal infringements, the protection of the peace and safety of mankind, as well as the prevention of crimes.

2. For the implementation of these objectives, the present Code establishes the bases for criminal liability, and defines what acts, which are dangerous for a person, society, or the state, shall be recognised as crimes, and establishes punishments and other measures of criminal-legal retribution for their commission.

Article 3. The Basis for Criminal Liability

The only basis for criminal liability shall be the commission of a crime, that is, an act which has all of the attributes of a legally defined crime stipulated by the present Code. No one can be subject to repeated criminal liability for one and the same crime.

Article 4. The Action of the Criminal Code in Time

The criminality and punishability of an act shall be defined by the law which was in effect during the time of the commission of that crime. The time of the commission of a socially dangerous act (failure to act), irrespective of the time of the emergence of consequences, shall be recognised as the time of the commission of a given crime.

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