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Biomedical subjects

Gerald D Buckberg

Publications and source records attributed to Gerald D Buckberg.

At least 37 records · Page 2Linked to original sources
PubMed2006

Myocardial protection in the failing heart: I. Effect of cardioplegia and the beating state under simulated left ventricular restoration.

OBJECTIVE: Heart failure was induced by cardiac pacing to evaluate myocardial flow distribution of the open ventricle during delivery of either cardioplegia or in the beating state during simulated left ventricular restoration. METHODS: Studies included 5 (pacing-induced) failing pig hearts and 6 control hearts. Pacing-induced cardiac failure reduced fractional shortening by approximately 22%, increased left ventricular end-diastolic diameter by 34%, caused pulmonary hypertension (mean blood pressure increased from 12 to 35 mm Hg), and led to significant ascites. Global and regional coronary blood flow were measured with microspheres during cardiopulmonary bypass at 80 mm Hg perfusion pressure in either vented (collapsed) or open (exposure by traction for left ventricular restoration) left ventricles during continuous perfusion under either beating-heart or cardioplegic conditions. RESULTS: In control hearts, venting and exposure ventriculotomy did not affect flow. In failing hearts decompressed by venting, coronary flow was lower during the beating and cardioplegic delivery than during control conditions at the same perfusion pressure of 80 mm Hg. Mean cardioplegic flow during ventricular decompression by venting exceeded beating flow by 97%. Conversely, traction to increase the ventricular radius during exposure ventriculotomy reduced endocardial cardioplegic coronary blood flow by 64% (from 0.97 to 0.59 mL/[min x g]), whereas the beating state raised endocardial flow by 95% (from 0.40 to 0.78 mL/[min x g]). Changing ventricular shape changed coronary vascular resistance in failing hearts during beating or cardioplegic delivery. CONCLUSIONS: Coronary blood flow alterations occurred only in failing hearts when geometry was changed from closed to open state. The beating method provided more endocardial flow than cardioplegic delivery during ventricular exposure for restoration. Vascular remodeling raised coronary vascular resistance in failing hearts, thereby requiring higher pressure for similar blood flows.

Animals↗
PubMed2006

Myocardial protection in the failing heart: II. Effect of pulsatile cardioplegic perfusion under simulated left ventricular restoration.

OBJECTIVE: The open ventricle was studied in pacing-induced experimental heart failure to determine the extent of coronary perfusion and distribution during either continuous or pulsatile cardioplegic perfusion compared with whole blood in the beating heart. METHODS: In 5 animals that underwent pacing-induced heart failure and in 6 control swine, regional coronary blood flows were measured on bypass in the open left ventricle (simulating exposure for left ventricle restoration) during (1) beating, (2) nonpulsatile cardioplegia, and (3) pulsatile cardioplegia modalities. Mean perfusion pressure was maintained at 80 mm Hg. RESULTS: Flow magnitude and distribution differed in control and failing hearts in the open left ventricle. In control hearts, transmural and endocardial cardioplegic flow of nonpulsatile and pulsatile flow (which were similar to each other) exceeded beating flow by 63% and 70%, respectively, in the open left ventricle condition. Transmural and subendocardial vascular resistance increased in failing hearts during cardioplegic delivery, resulting in lower subendocardial flow under nonpulsatile conditions for the same perfusion pressure. In failing hearts, subendocardial perfusion conditions did not change in the beating state (0.89 vs 0.78 mL/min/g in control and failing open beating states, respectively), but nonpulsatile cardioplegic flow was significantly reduced by 154%, and became lower than beating flow by 32.2% (0.78 vs 0.59 mL/min/g). Conversely, pulsatile cardioplegic delivery improved endocardial flow in the open failing hearts, as cardioplegic perfusion with pulsatility exceeded beating flow by 41%. In heart failure, pulsatility from either the beating heart, which causes extrinsic compression of coronary vessels, or intrinsic vessel distension during pulsatile cardioplegic perfusion preserved endocardial perfusion better than nonpulsatile cardioplegia at the same perfusion pressure. CONCLUSION: In the failing open ventricle (simulated geometry during ventricular restoration), subendocardial blood flow was maintained in the beating state, but decreased significantly from control values during nonpulsatile cardioplegic perfusion. Conversely, pulsatile cardioplegic delivery improved subendocardial perfusion of the open failing ventricle. These findings of improved subendocardial perfusion during pulsatile delivery (either during beating or cardioplegic perfusion) compared with nonpulsatile cardioplegic delivery may have important implications for myocardial protection in failing hearts.

Animals↗
PubMed2005

Neurologic preservation by Na+-H+ exchange inhibition prior to 90 minutes of hypothermic circulatory arrest.

BACKGROUND: The effects of pretreatment with cariporide (HOE 642 Aventis Pharma, Strasbourg-Cedex, France), a Na+-H+ exchanger (NHE) blocker, were studied in a cerebral ischemia-reperfusion model of hypothermic arrest. METHODS: Fifteen Yorkshire-Duroc pigs (37.1 +/- 4.2 kg) underwent femoral-jugular bypass and 90 minutes of deep hypothermic circulatory arrest at 19 degrees C. Ten animals were untreated, whereas 5 received 5 mg/kg of intravenous cariporide before cooling. After rewarming and off cardiopulmonary bypass, the pigs were weaned from anesthesia and followed for 24 hours. A standardized neurologic scoring system assessed brain functional recovery. Biochemical markers were used to analyze cellular injury. Control studies without circulatory arrest were done in 2 animals that underwent similar cooling and rewarming. RESULTS: Neurologic recovery was rapid and complete in the nonischemic controls and in all pretreated animals. Conversely, at 24 hours, all untreated pigs exhibited a cloudy or stuporous level of consciousness, abnormal positioning, and with only one exception, could not sit or stand. The gradation of neurologic score (evaluating central nervous system, motor and sensory functions, respiration condition, level of consciousness, and behavior) was 0 +/- 0 (0 = normal, 500 = brain death) in the treated group, compared with 124 +/- 59 in the untreated animals. Biochemical analysis showed every variable of whole-body injury (including conjugated dienes (p < 0.05), serum aspartate amino transferase (p < 0.01), creatine kinase p < 0.001) and endothelin-1 (p < 0.001) to be higher in the untreated group. CONCLUSIONS: NHE function alters experimental brain ischemia-reperfusion damage. These observations imply that NHE inhibition therapy before ischemia may improve neurologic protection in adult and infant patients undergoing cerebral ischemia during procedures that use hypothermic circulatory arrest.

Animals↗
PubMed2005

Architecture must document functional evidence to explain the living rhythm.

The central theme of surgical procedures is to interact structure and function. Two reviews of architecture by Torrent-Guasp and Lunkenheimer provide anatomic observations, and then only deduce, rather than test and verify functional relationships. Lunkenheimer previously showed the reciprocal helical configuration of the connective tissue scaffold, a weave-like network that may be the lattice for the descending and ascending segments of Torrent-Guasp's apical loop formed from the helical band. Lunkenheimer stresses cardiac development from a blood vessel, and exposes the need to disregard heart formation by a band that develops between the pulmonary artery and aorta. Torrent-Guasp's band-like concept is confirmed by MRI and sonomicrometer measurements, together with early systolic filling by ongoing, unopposed contraction of the ascending segment of the apical loop. This muscular component contradicts conventional concepts that elastic recoil causes rapid ventricular filling. However, direct physiologic measurements show that Torrrent-Guasp's physiologic timing sequence must be revised. While presumption is an important first step, proof of the marriage of structure and function happens only with measurement, a critical step before surgical action.

Biomechanical Phenomena↗
PubMed2005

Structure function interface with sequential shortening of basal and apical components of the myocardial band.

OBJECTIVE: To mechanically test the intact cardiac structure to determine the sequence of contraction within the myocardial mass to try to explain ejection and suction. METHODS: In 24 pigs (30-85 kg), segment shortening at the site of sonomicrometer crystals was continuously recorded. The ECG evaluated rhythm, and Millar pressure transducers measured intraventricular pressure and dP/dt. RESULTS: Study of segment shortening defined a sequence of contraction within the myocardial mass, starting at the free wall of the right ventricle and on the endocardial side of the antero-septal wall of the left. Crystal location defined underlying contractile trajectory; transverse in right ventricle followed by basal posterior left ventricle, and from the endocardial anterior wall to the posterior apical segment and finally to the epicardial side of the anterior wall. Mean shortening fraction averaged 18+/-3%, with endocardial exceeding epicardial shortening by 5+/-1%. Epicardial segment crystal displacement followed endocardial shortening by 82+/-23 ms in the anterior wall, and finished 92+/-33 ms after endocardial shortening stopped, time frame that matches the interval of fast drop of ventricular pressure and the start of suction. CONCLUSIONS: Crystal shortening fraction sequence followed the rope-like myocardial band model to contradict traditional thinking, with two starting points of excitation-contraction, the right anterior free wall of the right ventricle, and the endocardial side of the anterior wall. Active suction may be due to active shortening of the epicardial fibers of the anterior wall, because relaxation was not detected when both mitral and aortic valves were closed during the interval previously termed 'isovolumetric relaxation'.

Animals↗
PubMed2004

Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation.

OBJECTIVES: The purpose of this study was to test how surgical ventricular restoration (SVR) affects early and late survival in a registry of 1,198 post-anterior infarction congestive heart failure (CHF) patients treated by the international Reconstructive Endoventricular Surgery returning Torsion Original Radius Elliptical shape to the left ventricle (RESTORE)team. BACKGROUND: Congestive heart failure may be caused by late left ventricular (LV) dilation after anterior infarction. The infarcted segment is often akinetic rather than dyskinetic because early reperfusion prevents transmural necrosis. Previously, only dyskinetic areas were treated by operation. Surgical ventricular restoration reduces LV volume and creates a more elliptical chamber by excluding scar in either akinetic or dyskinetic segments. METHODS: The RESTORE group applied SVR to 1,198 post-infarction patients between 1998 and 2003. Early and late outcomes were examined, and risk factors were identified. RESULTS: Concomitant procedures included coronary artery bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality after SVR was 5.3% (8.7% with mitral repair vs. 4.0% without repair; p < 0.001). Perioperative mechanical support was uncommon (<9%). Global systolic function improved postoperatively. Ejection fraction (EF) increased from 29.6 +/- 11.0% preoperatively to 39.5 +/- 12.3% postoperatively (p < 0.001). The left ventricular end-systolic volume index (LVESVI) decreased from 80.4 +/- 51.4 ml/m(2) preoperatively to 56.6 +/- 34.3 ml/m(2) postoperatively (p < 0.001). Overall five-year survival was 68.6 +/- 2.8%. Logistic regression analysis identified EF or=80 ml/m(2), advanced New York Heart Association (NYHA) functional class, and age >or=75 years as risk factors for death. Five-year freedom from hospital readmission for CHF was 78%. Preoperatively, 67% of patients were NYHA functional class III or IV and postoperatively, 85% were class I or II. CONCLUSIONS: Surgical ventricular restoration improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent five-year outcome.

Aged↗
PubMed2004

Ventricular restoration--a surgical approach to reverse ventricular remodeling.

Congestive heart failure is most often caused by scar from coronary occlusion. The transition from occluded vessel to scar to dilation results in a remodeled ventricle that changes shape from ellipse to sphere. This shape change following an index event is called remodeling and a surgical approach for restoration (bring back to normal) will be described that uses the patient's own tissue, rather than employing heart replacement by mechanical devices or transplantation. The surgical restoration approach was taken by the RESTORE group that comprises an international medical and surgical team that will report (a) the remodeling infrastructure, role of compensatory remote muscle, and factors underlying surgical restoration decisions, (b) structural basis for ventricular geometric changes and surgical background for restoration, (c) individual rebuilding experience in 1150 patients over 20 years from one center, (d) integrated 5 year results from the RESTORE team in 1198 patients, (e) electrical aspects of restoration in 382 patients with only one AICD used, (f) how restoration improves mechanical synchrony without electrical devices, (g) geometric reasons for secondary mitral insufficiency and impact of adding mitral repair during SVR procedures, and (h) importance of defining site specific scar in no ischemic disease to identify a similar trigger lesion in non ischemic cardiomyopathy. The importance of a team approach by the RESTORE group may set the benchmark for collaborative world wide groups, and thereby depart from traditional focal approaches by individual disciplines.

Endocardium↗
PubMed2004

Heart failure following anterior myocardial infarction: an indication for ventricular restoration, a surgical method to reverse post-infarction remodeling.

Anterior myocardial infarction produces abrupt left ventricular (LV) dysynergy and global systolic dysfunction. Rapid intense neurohumoral activation, infarct expansion, and early ventricular chamber dilatation all contribute to restoring a normal stroke volume despite a persistently depressed ejection fraction. Continued neurohumoral activation provokes late remodeling of the remote non-infarcted myocardium, characterized by an abnormal progressively increasing LV volume/mass ratio that leads to further LV remodeling. Heart failure is a progressive disorder of LV remodeling. Heart failure from post-infarction remodeling is unique because of the persistent non-functioning scar that self- perpetuates abnormal loading conditions and neurohumoral activation. Medical therapy attenuates remodeling and improves survival but does not change the size of the scar. Surgical ventricular restoration to exclude the non-functioning infarct from the ventricular cavity decreases ventricular volumes, increases global ejection fraction, attenuates neurohumoral activation and yields an excellent 5-year survival. Combined medical and surgical therapy is recommended in this patient population.

Endocardium↗
PubMed2004

Surgical ventricular restoration: the RESTORE Group experience.

Congestive heart failure may be caused by late left ventricular (LV) dilation following anterior infarction. Early reperfusion prevents transmural necrosis, and makes the infarcted segment akinetic rather than dyskinetic. Surgical ventricular restoration (SVR) reduces LV volume and creates a more elliptical chamber by excluding scar in either akinetic or dyskinetic segments. The international RESTORE group applied SVR in a registry of 1198 post-infarction patients between 1998 and 2003. Early and late outcomes were examined and risk factors identified.Concomitant procedures included coronary artery bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality after SVR was 5.3% (8.7% with mitral repair vs. 4.0% without repair, p < .001) Perioperative mechanical support was uncommon (< 9%). Global systolic function improved postoperatively, as ejection fraction increased from 29.6 +/- 11.0% to 39.5 +/- 12.3% (p < .001) and left ventricular end systolic volume index decreased from 80.4 +/- 51.4 ml/m(2) to 56.6 +/- 34.3 ml/m(2) (p < .001). Overall 5-year survival was 68.6 +/- 2.8%, Logistic regression analysis identified EF < or = 30%, LVESVI > o = 80 ml/m(2), advanced NYHA functional class, and age > or =75 years as risk factors for death. Five-year freedom from hospital readmission for CHF was 78%. Preoperatively, 67% of patients were class III or IV, and postoperatively 85% were class I or II.SVR improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent 5-year outcome.

Aged↗
PubMed2004

Reduction of systolic and diastolic dysfunction by retrograde coronary sinus perfusion during off-pump coronary surgery.

OBJECTIVES: We evaluated the protective effects of retrograde coronary sinus perfusion to offset potential systolic and diastolic dysfunction (myocardial stunning) after temporary regional ischemia needed for off-pump coronary artery bypass grafting. METHODS: Twenty Yorkshire-Duroc pigs (31.8 +/- 3.9 kg) underwent 15 minutes of mid-left anterior descending coronary artery ischemia in the beating heart. In 8 pigs, no protective measures were used. In 12 pigs, an aorta-coronary sinus shunt (with conventional cannulas) allowed retrograde perfusion during temporary ischemia; in 6 of these pigs, no leakage to the right atrium was ensured. Regional endocardial contraction was measured with sonomicrometer crystals. Systolic dysfunction (impaired regional shortening), diastolic dysfunction (contraction extending into early diastole), and coronary sinus nitric oxide and endothelin-1 levels were recorded. RESULTS: Before ischemia, contraction did not extend into the diastolic interval. During ischemia, paradoxic bulging occurred in all hearts except in the occlusive coronary sinus shunt group (16% +/- 6% of baseline, P <.01). Sixty minutes after ischemia, systolic segment shortening recovered 36% +/- 24% without retrograde perfusion versus 56% +/- 20% and 61% +/- 14% with coronary sinus shunting (P <.05). Diastolic dysfunction (as percentage of diastolic time in contraction) was 38% +/- 16% in the nontreated group versus 22% +/- 22% and 9% +/- 9% (P <.05) after shunting and occlusive shunting, respectively. This correlated with a left ventricular end-diastolic pressure increase of 4 mm Hg in the ischemic group versus no change in the retrograde perfusion groups. Nitric oxide decreased 15% without shunting and increased 8% after occlusive coronary sinus shunting (P <.05). CONCLUSIONS: Retrograde coronary sinus perfusion during simulated off-pump coronary revascularization diminishes systolic and diastolic dysfunction. An aortic-coronary sinus shunt is a rapid, recognized approach that can improve myocardial muscle and endothelial safety during off-pump coronary artery bypass grafting.

Animals↗
PubMed2004

Stroke and extra-cardiac perfusion: new vantage points in brain protection.

This report shows a new spectrum of applications of a concept of brain protection for the cardiothoracic surgeon. The underlying treatment deals with an ischemic/reperfusion injury, and novel applications of principles well known in cardiac surgery will be used to provide brain protection. Unique opportunities arise from the uncommon use of circulatory arrest in infants and adults (1-2% of procedures) to the larger areas of sudden death (450,000 pts/year in the US), stroke (700,000 pts/year) and carotid occlusion for peri-operative endarterectomy, and neurologic problems after CPB (30% incidence). Treatment pathways in sudden death will address the brain during CPR, the body to get a cause of arrest with use of peripheral CPB, and a controlled cardiac reperfusate to correct the underlying lesion. Circulatory arrest provides the model to treat, both this uncommon surgical process, with extension as toward treating stroke with controlled reperfusion. Novel models of pretreatment and warm brain reperfusion, that mimic warm heart reperfusion are suggested. Construction of the ultimate brain reperfusate, and its conditions of delivery will follow the valid and tested development phases of a warm cardioplegic solution, but become directed towards the brain. Old tricks that lead to new goals will become our innovative vantage points.

Animals↗