Left Ventricular Power Failure Research Articles

Part 7: The Era of Reperfusion

Part 7: The Era of Reperfusion

Protection of evolving myocardial infarction and failed PTCA

Acute myocardial infarction is caused by acute coronary occlusion and is the major cause of death in Europe and the United States. In-hospital mortality is due principally to cardiogenic shock because of extensive ischemic muscle damage. Previous surgical results of coronary artery bypass grafting for left ventricular power failure have been disappointing because intraoperative ischemic injury is superimposed on severe damage already sustained by the myocardium. Surgical revascularization has, in general, been restricted to patients with acute occlusion after elective percutaneous transluminal coronary angioplasty with or without thrombolytic therapy. During the last years new knowledge has been gained in the pathophysiology of acute coronary occlusion on ischemic and nonischemic (remote) myocardium that has evolved in a new surgical strategy for revascularization of patients with evolving myocardial infarctions and failed percutaneous transluminal coronary angioplasty. Studies of the natural history of acute regional ischemia have shown that acute occlusion of a coronary artery not only affects the ischemic myocardium but causes structural, functional, and metabolic alterations in the remote and adjacent myocardium. These changes in the remote myocardium are even more severe if the remote myocardium is supplied by a stenotic coronary artery. Furthermore, many experimental and clinical studies have shown that normal blood reperfusion of myocardium injured previously by ischemia leads to additional damage (reperfusion injury).(ABSTRACT TRUNCATED AT 250 WORDS)

Does ventricular fibrillation cause myocardial stunning during defibrillator implantation?

Induction of ventricular fibrillation (VF) is an important part of the process of inserting implantable cardioverter defibrillators (ICDs), allowing the measurement of defibrillation thresholds. However, animal studies have revealed that repeated cycles of VF and defibrillation result in depressed left ventricular (LV) function and reduced cardiac output. Short intervals of VF do not affect myocardial contractility but longer periods produce heart failure. Induced VF was used in a canine model to study profound myocardial stunning leading to heart failure, as well as the therapeutic potential of the phosphodiesterase inhibitor, amrinone (combined with epinephrine and norepinephrine). Amrinone was found to significantly (p < 0.05) increase contractility when added to a stable preparation supported by epinephrine and norepinephrine infusion; amrinone or catecholamines alone had no effect. In the clinical setting, the following factors may affect LV contractility during ICD surgery: catecholamines released as a result of hypotension; negative VF; ischemia; antiarrhythmic drugs; anesthetics; and bradycardia after device testing. Patients (n = 125) have tolerated ICD insertion well. Early data reveals no significant changes in ejection fraction. Though rare, death due to myocardial stunning and LV power failure can occur during ICD insertion. It may be possible to use arterial pressure monitoring to predict this event in vulnerable patients.

Studies on prolonged acute regional ischemia: VI. Myocardial infarction with left ventricular power failure: A medical/surgical emergency requiring urgent revascularization with maximal protection of remote muscle

Eighty consecutive patients receiving maximum inotropic and intraaortic balloon support underwent emergency coronary artery bypass grafting 3.4 +/- 1 days (mean +/- standard error) after infarction for severe left ventricular power failure (stroke work index less than 25 gm-m, left atrial pressure greater than 20 mm Hg). All underwent induction of cardioplegia with a 37 degrees C glutamate/aspartate blood cardioplegic solution, multidose cold (4 degrees C) replenishment, and warm reperfusate. Viable areas were grafted first to ensure cardioplegic distribution. Left ventricular power failure was reversed in 94% of patients; 75 of 80 patients had discontinuation of inotropic drugs and intraaortic balloon support. The early mortality rate (less than 30 days) was only 7% (3/45) with early operation (less than 18 hours) and rose to 31% (11/35, p less than 0.05) if operation was delayed more than 18 hours. Six of 14 early deaths were due to progression of preoperative organ failure despite reversal of shock. Eighteen of 66 early survivors died of end-stage heart failure (21/80), a 26% late mortality rate. Nonsurvivors (early and late) had a higher incidence of extending versus evolving infarction (33/64 versus 2/16, p less than 0.05), a longer delay from shock to operation (11/45 versus 24/35, p less than 0.05), more preoperative organ failure (9/9 versus 26/71, p less than 0.05), and a greater incidence of previous infarction (22/43 versus 13/37, p greater than 0.05). Thirty of 45 late survivors (67%) remain physically active. We conclude that left ventricular power failure should be considered a medical/surgical emergency that necessitates prompt angiography and can be reversed in selected patients. Postoperative mortality (early and late) is due principally to delay of operation leading to progression of preoperative organ failure or progression of underlying cardiac disease if infarction becomes established.

Studies on prolonged acute regional ischemia: V. Metabolic support of remote myocardium during left ventricular power failure

This study tests the hypothesis that metabolic support of remote "nonischemic" myocardium during acute infarction will reverse the trend toward cardiogenic shock. Thirty-seven dogs underwent ligation of the left anterior descending coronary artery and 50% stenosis of the circumflex coronary artery. Irreversible ventricular fibrillation developed in 11 of them. The 26 survivors were observed for up to 6 hours; global and regional left ventricular function (cardiac index, stroke work index, ultrasonic crystals) and regional blood flow (radioactive microspheres) were measured. After 2 hours, eight dogs received an intravenous infusion of glutamate/aspartate, glucose-insulin-potassium, coenzyme Q10, and 2-mercapto-propionyl-glycine for 4 hours. Five dogs received the mannitol infusion to raise serum osmolarity 30 mOsm. Four additional dogs received the intravenous substrate infusions over 4 hours without undergoing ischemia. The substrate infusion for 4 hours caused no change in regional or global cardiac function in the four control dogs. Three of nine untreated dogs died of cardiogenic shock, and progressive left ventricular power failure occurred in the six others (40% decrease in cardiac index, 50% decrease in stroke work index, p less than 0.05) because of persistent dyskinesia in the left anterior descending region (-40% of systolic shortening, p less than 0.05) and hypocontractility in the circumflex region (48% of control systolic shortening, p less than 0.05), despite normal transmural blood flow in the posterior left ventricular wall (76 ml/100 gm/min). In contrast, in treated dogs, hypercontractility recovered in the circumflex segment (138% of systolic shortening) and stroke work index rose to control levels (91%) without a change in regional blood flow. Mannitol infusion did not improve hemodynamics or avoid the development of progressive left ventricular power failure. We conclude that cardiogenic shock after myocardial infarction is due, in large part, to impaired ability of "nonischemic" myocardium to maintain hypercontractility. This limitation can be prevented by metabolic support of viable muscle, and the data imply that intravenous substrate infusions may be helpful before definitive treatment (i.e., coronary artery bypass grafting) is undertaken.

Studies on prolonged acute regional ischemia: IV. Aggressive surgical treatment for intractable ventricular fibrillation after acute myocardial infarction

Of 21 dogs undergoing ligation of the left anterior descending coronary artery and 50% stenosis of the left circumflex coronary artery, 15 developed intractable ventricular fibrillation and underwent 1 added hour of femoro-femoral bypass. Three hearts were removed after 1 hour on bypass without myocardial reperfusion for biochemical and mitochondrial analysis. After the 1 hour, five underwent unmodified blood reperfusion on bypass; seven underwent 1 hour of aortic clamping on vented bypass to simulate coronary artery bypass grafting with multidose blood cardioplegic reperfusion. Regional systolic shortening was measured with ultrasonic crystals and cardiac output was measured by thermodilution techniques. All six hearts with no ventricular fibrillation or with reversible ventricular fibrillation and hearts that were not reperfused developed cardiogenic shock (40% decrease in stroke work index, p less than 0.05) because of persistent left ventricular dyskinesia (-40% of systolic shortening, p less than 0.05) and progressive circumflex hypocontractility (48% systolic shortening, p less than 0.05) and showed extensive (68%) triphenyltetrazolium chloride nonstaining. Two dogs died of left ventricular power failure (33% mortality rate). In contrast, 11 of 12 dogs that were reperfused could be weaned from bypass (8% mortality rate). The four dogs surviving after unmodified blood reperfusion (20% mortality rate) showed severe residual left ventricular dysfunction (39% of control stroke work index, p less than 0.05), had equivocal recovery of anterior contractility (10% +/- 7% of systolic shortening), had marginal recovery of contractility in the remote myocardium (60% +/- 11% of systolic shortening), and had extensive triphenyltetrazolium chloride nonstaining (58%). Conversely, all seven dogs with intractable ventricular fibrillation undergoing controlled reperfusion after 4 hours of ischemia recovered normal stroke work index (91%), regained 23% of systolic shortening in the region supplied by the left anterior descending coronary artery (p less than 0.05), 125% of systolic shortening in the circumflex region (p less than 0.05), and showed only 25% triphenyltetrazolium chloride nonstaining (p less than 0.05). These results suggest aggressive treatment of intractable ventricular fibrillation after acute myocardial infarction by providing reperfusion on bypass can salvage hearts thought previously to be damaged irreversibly.(ABSTRACT TRUNCATED AT 400 WORDS)

Percutaneous intraaortic balloon pumping: four years from Tiblisi.

Intraaortic balloon pumping (IABP) has now evolved as the mechanical supportive treatment of choice for the management of refractory left ventricular power failure. A new single-chambered percutaneous intraaortic balloon (Datascope Corp., Paramus, NJ, U.S.A.) has been constructed around a central guidewire. The balloon can be wrapped around the guidewire, enabling its insertion into the femoral artery through a 12-F sheath, inserted by a modified Seldinger technique. A dual-lumen automatic wrapping version has recently been employed. Percutaneous IABP insertion has been performed in 149 patients (mean age 58 years). In our medical group of 75 patients, 59 underwent urgent open heart surgery and 53 (90%) survived. In patients who could not be separated from cardiopulmonary bypass, 23 of 61 (38%) survived. Vascular complications occurred in 10% of the patients. Percutaneous balloon insertion permits the rapid institution of IABP support and broadens the medical and surgical applications of IABP.

Surgical repair of remediable postinfarction cardiogenic shock in the elderly. Early and long-term results.

The in-hospital mortality associated with acute myocardial infarction rises markedly with advancing age. It is not established whether the elderly may benefit from early surgical repair of postinfarction cardiogenic shock due to ventricular septal defect (VSD), acute severe mitral regurgitation (MR), or left ventricular power failure. Eighteen consecutive patients between the ages of 66 and 79 (mean, 72 years) and in cardiogenic shock underwent surgical repair, most with counterpulsation support, within one week of developing VSD, MR, or left ventricular power failure. Of ten patients with VSD, five (50%) survived. Three of seven patients with MR (43%) and the only patient with power failure survived for an overall survival of 50%. The nine long-term survivors were followed up for six months to five years (mean 31 months) by personal interviews with the patient or referring physician. There was one late death, due to congestive heart failure, ten months after the operation. Of the remaining eight patients, seven are categorized as New York Heart Association class I, and one as class II. These patients have all been able to live and function independently after cardiac operation. The authors conclude that older patients with postinfarction cardiogenic shock may benefit from early operation and that advanced age does not preclude successful surgical outcome. Furthermore, operation may result in excellent long-term quality of life.

Warm induction of cardioplegia with glutamate-enriched blood in coronary patients with cardiogenic shock who are dependent on inotropic drugs and intra-aortic balloon support: Initial experience and operative strategy

This report reviews the initial clinical application of our experimental studies inducing cardioplegia with a warm (37 degrees C) glutamate-enriched blood solution in ischemically damaged hearts. Over 15 months, 23 consecutive coronary patients requiring preoperative intra-aortic balloon and inotropic drug support for cardiogenic shock underwent operation for left ventricular power failure. Twelve patients were given a warm glutamate-enriched blood cardioplegic solution during the first 5 minutes of aortic clamping before multidose cold (4 degrees C) glutamate blood cardioplegia was begun; 11 patients received standard multidose cold blood cardioplegia without glutamate. All patients had comparably depressed left ventricular performance preoperatively despite maximal inotropic and balloon support and showed evidence of extending myocardial infarction. They did not differ in the number of grafts placed (3.7 +/- 0.2), associated valve and aneurysm procedures (seven patients) or cross-clamp time (89 +/- 6 minutes). All patients received warm blood cardioplegic reperfusion before aortic unclamping. The perioperative mortality was 9% (2/23); both patients who died received cold blood cardioplegia without glutamate. In addition to lower mortality, patients receiving warm glutamate blood cardioplegia exhibited better hemodynamics, allowing earlier discontinuation of inotropic drug infusion (1.3 +/- 0.5 versus 2.7 +/- 0.8 days, p less than 0.05) and intraaortic balloon support (1.2 +/- 0.2 versus 3.6 +/- 0.5 days, p less than 0.05). Late mortality was 30%, resulting in a 65% overall survival rate (2 to 15 months) for the entire series of patients. The operative principles evolving from this early experience include (1) warm blood cardioplegic induction, (2) glutamate enrichment, (3) meticulous attention to cardioplegic distribution and grafting sequence, (4) warm cardioplegic reperfusion before unclamping, and (5) graft perfusion during construction of proximal anastomoses. Hopefully, further application of these techniques will improve results in these extremely high risk coronary patients requiring operation.

Emergency Guidelines for AVCO/Datascope Intraaortic Balloon Pump Console Substitution

Intraaortic balloon pumping is widely utilized for mechanical circulatory support of patients with left ventricular power failure. Although intraaortic balloon pump consoles are quite reliable, malfunctions do occur. If a standby console of similar make is not available, a console of a different manufacturer can be utilized to continue counterpulsation. This article provides guidelines for the emergency driving of a Datascope pump console and an AVCO balloon catheter, and an AVCO pump console and a Datascope balloon catheter. The successful use of the Datascope pump and an AVCO balloon in 5 patients is reported.

Indications and limitations of IABP for severe left ventricular power failure

Indications and limitations of IABP for severe left ventricular power failure

Left ventricular mechanics of counterpulsation and left heart bypass, individually and in combination

Counterpulsation and left heart bypass devices have been successfully used to salvage patients with severe left ventricular power failure following cardiopulmonary bypass. Each of these techniques is believed to reduce or minimize myocardial work, yet the effects of these devices on the force of myocardial contraction have not been defined. In the present investigation the effects of counterpulsation produced by intravascular (intra-aortic balloon pumping) and extravascular (pulsatile assist device) balloon devices, partial left atrial-aortic bypass, and total bypass on left ventricular mechanics were examined. The devices were studied individually and in combination in 10 anesthetized open-chest dogs. Left ventricular wall stress, external work, and contractility indices were calculated by computer using a changing volume spherical model of the left ventricle. Results indicate that although all currently available circulatory assist devices reduced peak left ventricular wall stress, a spectrum of relative effectiveness progressed from intra-aortic balloon pumping or pulsatile assist device alone through the combination intra-aortic balloon pumping plus the pulsatile assist device. Partial left heart bypass was more effective than intra-aortic balloon pumping plus the pulsatile assist device in reducing peak wall stress, but the difference was small. Total left heart bypass was vastly superior to any of the other modalities tested in its effects on peak wall stress as well as external work. The addition of counterpulsation to partial or total left heart bypass produced minimal changes in left ventricular systolic mechanics.

The chest x-ray in acute left ventricular power failure: an aid to determining prognosis of patients supported by intraaortic balloon pumping

Serial chest x-rays were used as a means of evaluating the hemodynamic status of 43 patients in acute left ventricular power failure (LVPF) complicating acute myocardial infarction who were assisted with balloon pumping. The following findings were reported: 1. In patients with acute myocardial infarction, prediction of the hemodynamic status on the basis of chest x-rays is less reliable when severe LVPF is present as a complication. 2. The incidence and severity of roentgenographic findings of congestive heart failure and pulmonary edema are increased in patients with severe LVPF compared to patients with uncomplicated myocardial infarction. 3. Improvement in the roentgenographic degree of heart failure with positive clinical and hemodynamic responses to 24 hr or less of balloon pumping is an indication that patients in severe acute LVPF may survive. Patients with deteriorating or unchanging chest x-ray findings have an extremely poor prognosis. These patients should be evaluated by cardiac catheterization and coronary arteriography to determine the appropriateness of emergency surgical correction.

Ascending Aorta Insertion of the Dual-Chambered Intraaortic Balloon for Counterpulsation During Cardiac Operations

A patient with left ventricular power failure after aortocoronary saphenous vein bypass was successfully managed by intraaortic dualchambered balloon counterpulsation through the ascending aorta. This insertion route reverses the orientation of the spherical distal chamber, which inflates early in diastole and partially occludes the aorta. This position achieved an effective augmentation pressure during left ventricular diastole and reduced arterial end-diastolic pressure considerably. The technique of insertion and events at operation and postoperatively are discussed.

Intraoperative unidirectional intra-aortic balloon pumping in the management of left ventricular power failure

Unidirectional intra-aortic balloon pumping (IABP) was applied to 28 adult patients undergoing open-heart surgery over a 35 month period. The patients were divided into three groups according to the temporal sequence of initiating IABP. Group A consisted of 4 patients who were in a low output state or in cardiogenic shock prior to study. All patients survived cardiac catheterization and surgery, and 3 (75 per cent) were long-term survivors. Group B included 15 patients who could not be weaned from cardiopulmonary bypass with the usual supportive measures. Twelve patients (80 per cent) were weaned from bypass with IABP, and 11 (73 per cent) were discharged from the hospital. Group C was composed of 9 patients who manifested a low cardiac output syndrome within the first 24 hours following surgery. IABP was initiated in the recovery room. Six patients (67 per cent) were discharged. The total experience with these 28 patients therefore includes 24 patients (86 per cent) who were weaned from IABP, 20 (71 per cent) who were discharged, and 18 (64 per cent) who were long-term survivors. The present criteria for the use of IABP in the cardiac surgical patient are defined.

Patient selection for cardiac surgery in left ventricular power failure.

Nineteen patients in acute left ventricular power failure following acute myocardial infarction were given support with intraaortic balloon pumping and underwent cardiac catheterization. Hemodynamic response to disastolic augmentation, results of left ventriculography, and observations of selective coronary arteriography were evaluated to determine which patients could survive without operation, which would require operation to survive, and which could be predicted not to survive operation. Of ten patients who underwent operation, three were long-term survivors. Two patients predicted to have a good prognosis without surgery did survive. Of three patients who had been determined to require operation but not undergo it, two died in the hospital and one a month later. The four patients whose conditions were considered inoperable died in the hospital. The results indicate that current methods of predicting the need for corrective surgery are relatively accurate and that the rate of survival in surgically treated patients may be increased.

Intra-aortic balloon counterpulsation. Indications and long-term results in postoperative left ventricular power failure.

Intra-aortic balloon counterpulsation is an effective treatment for left ventricular power failure after cardiopulmonary bypass. This report delineates our experience with 12 patients, nine men and three women. All patients required counterpulsation after reconstructive surgery for severe coronary artery disease. The average time of counterpulsation was 3.9 days, and 50% of the patients were weaned from counterpulsation in less than three days. Seven patients (60%) were discharged from the hospital. There were two late deaths. The five long-term survivors (42%) have enjoyed good to excellent rehabilitation at nine to 31 months.

Left ventricular and unidirectional intra-aortic balloon pumping: Effects on hemodynamics in canine cardiogenic shock

Intra-aortic balloon pumping (IABP) is currently the supportive treatment of choice for the management of refractory left ventricular power failure. However, in the extremely low output state, IABP may be hemodynamically ineffective, and a more direct left ventricular assist is desirable. Left ventricular balloon pumping (LVBP) is an effective cardiac assist device in the experimental low output state. LVBP both alone and in combination with IABP was evaluated in an experimental canine cardiogenic shock preparation. With LVBP alone, significant improvement was seen in the following: mean aortic flow (AoF), +46.2 per cent; aortic pressure (AoP), +15.1 per cent; left ventricular stroke work (LVSW), +147.0 per cent; left ventricular dp/dt (LVdp/dt), +52.9 per cent; coronary sinus flow (CSF), +24.6 per cent; and myocardial oxygen consumption +25.2 per cent. There was a concomitant decrease in left ventricular end-diastolic pressure (LVEDP) -71.6 per cent and left atrial pressure (LAP) -62.7 per cent. The combination of LVBP and IABP showed further improvement in CSF (+6.1 per cent) and further decreases in LVdp/dt (-8.7 per cent), LVEDP (-48.0 per cent), LAP (-28.9 per cent) and myocardial oxygen consumption (-33.3 per cent). The results indicate that LVBP may be a promising circulatory assist and that, in the extremely low output state, the addition of IABP decreased myocardial oxygen consumption and offered a transition in mechanical cardiac support which was initiated with LVBP.

Iliac artery cannulation for intra-aortic balloon counterpulsation

A case of left ventricular power failure (LVPF) after coronary artery bypass was managed by intra-aortic balloon counterpulsation (IABCP) through the left common iliac artery. The technique of insertion is discussed.

Unidirectional balloon pumping in the inferior vena cava and aorta: Effects on canine hemodynamics in cardiogenic shock

Clinical applications of counterpulsation and, in particular, of intra-aortic balloon pumping (IABP) have been successful in the management of refractory left ventricular power failure. Synchronous external counterpulsation has emerged as an appealing noninvasive form of temporary cardiac assistance. To evaluate this modality, we performed 30 experiments in 6 dogs by inducing hypo- and hypervolemic cardiogenic shock with propranolol (1.5 mg. per kilogram) and ligation of the left anterior descending coronary artery (LAD). Unidirectional dual-chambered balloons were positioned in the inferior vena cava (IVCBP) and in the descending thoracic aorta (IABP) of the same animal to simulate external counterpulsation, and two assist consoles were synchronized to the electrocardiogram. The results indicate that IVCBP is detrimental in hypovolemic cardiogenic shock and that these results can be reversed with the addition of IABP. In contrast, IVCBP alone in hypervolemic cardiogenic shock resulted in significant hemodynamic improvement. It is concluded that the primary hemodynamic effects of these experiments, in which the venous hemodynamics of external counterpulsation have been simulated, may be related in great part to venous diastolic augmentation and to the state of hydration.