Left ventricular performance, regional blood flow, wall motion, and lactate metabolism during transluminal angioplasty. 1984

P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower

The response of left ventricular function, coronary blood flow, and myocardial lactate metabolism during percutaneous transluminal coronary angioplasty (PTCA) was studied in a series of patients undergoing the procedure. From four to six balloon inflation procedures per patient were performed with an average duration per occlusion of 51 +/- 12 sec (mean +/- SD) and a total occlusion time of 252 +/- 140 sec. Analysis of left ventricular hemodynamics in 19 patients showed that the relaxation parameters, peak negative rate of change in pressure, and early time constants of relaxation, responded earliest to short-term coronary occlusion (peak effect at 17 +/- 7 sec) while other parameters, such as peak pressure, left ventricular end-diastolic pressure, and peak positive rate of change in pressure, responded more gradually, suggesting a progressive depression of myocardial mechanics throughout the procedure. Left ventricular angiograms, available for 14 patients, indicated an early onset of asynchronous relaxation concurrent with the early response in peak negative dP/dt and the time constant of early relaxation. All hemodynamic functions fully recovered within minutes after the end of PTCA. Mean blood flow in the great cardiac vein and proximal coronary sinus and the hyperemic response were measured in 20 patients. Before PTCA mean flow in the great cardiac vein was 69 +/- 17 ml/min and in the coronary sinus it was 129 +/- 34 ml/min. Reactive hyperemia (great cardiac vein) was 55% after the first PTCA and 91% after the third. A more pronounced reaction was observed when the residual functional coronary stenosis was reduced in subsequent dilatations. Arteriovenous lactate difference appeared constant during the first two occlusions (control +0.11 mmol/liter, first PTCA -0.87 mmol/liter, and second PTCA -0.82 mmol/liter) and did not increase during subsequent occlusions. Within minutes after the procedure lactate balance was again positive, demonstrating the reversibility of the metabolic disturbances after repeated ischemia. The results of this study indicate that there is no permanent dysfunction of global or regional myocardial mechanics, myocardial blood flow, or lactate metabolism after PTCA with four to six coronary occlusions of 40 to 60 sec.

UI MeSH Term Description Entries
D007773 Lactates Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.
D009200 Myocardial Contraction Contractile activity of the MYOCARDIUM. Heart Contractility,Inotropism, Cardiac,Cardiac Inotropism,Cardiac Inotropisms,Contractilities, Heart,Contractility, Heart,Contraction, Myocardial,Contractions, Myocardial,Heart Contractilities,Inotropisms, Cardiac,Myocardial Contractions
D009206 Myocardium The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow. Muscle, Cardiac,Muscle, Heart,Cardiac Muscle,Myocardia,Cardiac Muscles,Heart Muscle,Heart Muscles,Muscles, Cardiac,Muscles, Heart
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D002306 Cardiac Volume The volume of the HEART, usually relating to the volume of BLOOD contained within it at various periods of the cardiac cycle. The amount of blood ejected from a ventricle at each beat is STROKE VOLUME. Heart Volume,Cardiac Volumes,Heart Volumes,Volume, Cardiac,Volume, Heart,Volumes, Cardiac,Volumes, Heart
D003326 Coronary Circulation The circulation of blood through the CORONARY VESSELS of the HEART. Circulation, Coronary
D003327 Coronary Disease An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels. Coronary Heart Disease,Coronary Diseases,Coronary Heart Diseases,Disease, Coronary,Disease, Coronary Heart,Diseases, Coronary,Diseases, Coronary Heart,Heart Disease, Coronary,Heart Diseases, Coronary
D006339 Heart Rate The number of times the HEART VENTRICLES contract per unit of time, usually per minute. Cardiac Rate,Chronotropism, Cardiac,Heart Rate Control,Heartbeat,Pulse Rate,Cardiac Chronotropy,Cardiac Chronotropism,Cardiac Rates,Chronotropy, Cardiac,Control, Heart Rate,Heart Rates,Heartbeats,Pulse Rates,Rate Control, Heart,Rate, Cardiac,Rate, Heart,Rate, Pulse
D006352 Heart Ventricles The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation. Cardiac Ventricle,Cardiac Ventricles,Heart Ventricle,Left Ventricle,Right Ventricle,Left Ventricles,Right Ventricles,Ventricle, Cardiac,Ventricle, Heart,Ventricle, Left,Ventricle, Right,Ventricles, Cardiac,Ventricles, Heart,Ventricles, Left,Ventricles, Right
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
September 1976, Medizinische Klinik,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
September 1980, Circulation,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
December 1986, Cardiologia (Rome, Italy),
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
June 2003, British journal of anaesthesia,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
September 1988, Journal of cardiology,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
September 1985, Journal of the American College of Cardiology,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
January 1977, Basic research in cardiology,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
June 1985, Journal of cardiography,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
April 2001, The American journal of cardiology,
P W Serruys, and W Wijns, and M van den Brand, and S Meij, and C Slager, and J C Schuurbiers, and P G Hugenholtz, and R W Brower
June 1983, International journal of cardiology,
Copied contents to your clipboard!