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Operative intra-aortic balloon rupture.

Rupture of an intra-aortic balloon (IAB), inserted to assist in weaning from cardiopulmonary bypass, occurred during attempted intra-aortic administration of protamine in a 71-year-old male who later died. Intra-aortic balloon counterpulsation (IABC) is most commonly utilized to assist in weaning from cardiopulmonary bypass (CPB) or to augment low-flow states following CPB. In-hospital survival following IAB insertion in these circumstances in patients with coronary artery disease is approximately 60 per cent. Patients with valvular disease have a lower in-hospital survival rate (50 per cent). Complications of IABC are usually of vascular or infectious origin. Balloon rupture is a rare though potentially lethal complication. The effects of balloon rupture may be compounded by the use of helium as a driving gas to inflate the balloon. Intra-aortic administration of protamine has not been shown to be superior to peripheral administration and should be avoided if an IAB is in place.

Aged↗

Incidence of gastrointestinal complications in cardiopulmonary bypass patients.

Gastrointestinal complications after cardiac surgery are associated with a high mortality rate. Because of the absence of early specific clinical signs, diagnosis is often delayed. The present study seeks to determine predictive risk factors for subsequent gastrointestinal complications after cardiosurgical procedures. Within a 1-year period, a total of 1116 patients who had undergone open heart surgery with cardiopulmonary bypass were prospectively studied for gastrointestinal complications. To determine predictive factors, all case histories of the patients were analyzed. Of the 1116 patients, 23 (2.1%) had gastrointestinal complications during the postoperative period, 10 of whom had to undergo subsequent abdominal surgery. Of these 23 patients, 20 died. Early gastrointestinal complications, which occurred mostly on postoperative days 6 or 7, consisted of bowel ischemia or hepatic failure. Late complications were gastrointestinal bleeding, pseudomembranous colitis, cholecystitis, and septic rupture of a spleen. The relative risk for abdominal complications after cardiopulmonary bypass was highly increased in association with (1) a cardiac index less than 2.0 l/min-1/(m2)-1, (2) postoperative onset of atrial fibrillation, (3) emergency surgery, (4) need for vasopressors, (5) need for intraaortic balloon counterpulsation, and (6) need for early redo thoracotomy due to surgical complications. All patients with necrotic bowel disease had elevated serum lactate levels. Furthermore, cardiopulmonary bypass and aortic clamping times were significantly prolonged in patients who developed gastrointestinal complications. A number of predictive factors contribute to the development of gastrointestinal complications after cardiopulmonary bypass surgery. Knowledge of these factors may lead to earlier identification of patients at increased risk and may allow more efficient and earlier interventions to reduce mortality.

Aged↗

[Sex, erectile dysfunction, and the heart: a growing problem].

BACKGROUND: Erectile dysfunction (ED) is defined as the inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance. ED may also be an early sign of cardiovascular disease. The main risk factors for coronary heart disease (high LDL, smoking, hypertension, diabetes) and ED are the same. ED after the diagnosis of coronary artery disease or myocardial infarction is also common. CARDIOVASCULAR EFFECTS AND RISK OF SEXUAL ACTIVITY: Cardiac and metabolic expenditures during sexual intercourse will vary depending on the type of sexual activity. When oxygen uptake was measured in men, an average metabolic expenditure during stimulation and orgasm of 2.5 metabolic equivalents (METs) was found for woman-on-top coitus, and of 3.3 METs for man-on-top coitus (range 2.0-5.4 METs). However, coital death is rare, encompassing only 0.6% of all sudden death cases. A retrospective case-crossover study has shown that although sexual activity can trigger the onset of myocardial infarction, the relative risk in the 2 h after sexual activity was low (2.5; 95% confidence interval [CI] 1.7-3.7). Sexual activity was a likely contributor to the onset of myocardial infarction only 0.9% of the time. Regular exercise appears to prevent triggering. It has to be cautioned that these reassuring data should not be extrapolated to patients taking sildenafil, if they perform at higher cardiac and metabolic expenditures during coitus. The hemodynamic changes associated with sexual activity may be far greater with an unfamiliar partner, in unfamiliar settings, and after excessive eating and drinking. The Princeton Consensus Table for estimation of cardiovascular risk during sexual intercourse gives a first orientation regarding the question which patients can perform sex safely and which subgroup needs further diagnosis and treatment. PHOSPHODIESTERASE-5 INHIBITORS FOR ED TREATMENT: The introduction of sildenafil has been a valuable contribution to the treatment of ED. Sildenafil acts as a selective inhibitor of cyclic guanosine monophosphate-(cGMP-)specific phosphodiesterase type 5 (PDE 5), resulting in smooth muscle relaxation, vasodilation, and enhanced penile erection. Reported cardiovascular side effects in healthy males are headache, flushing, and < 10% decreases in systolic and diastolic blood pressures. Significant hypotension can be found in patients who are concurrently taking nitrates. On the basis of the pharmacokinetic profile of sildenafil, the co-administration of a nitrate within the first 24 h is likely to produce a severe, potentially lifethreatening hypotensive response and is therefore contraindicated. The risk of precipitating a cardiotoxic, hypotensive, or hemorrhagic event secondary to combining sildenafil (a PDE 5 inhibitor) with specific PDE 3 inhibitors such as milrinone and enoximone or with nonspecific PDE inhibitors such as theophylline and pentoxifylline is unlikely. Sildenafil is predominantly metabolized by both the P450 2C9 pathway and the P450 3A4 pathway. Thus, potent inhibitors of the P450 3A4 pathway may increase the plasma concentrations of sildenafil, like cimetidine, erythromycin, digitoxin, and CSE inhibitors (simvastatin, atorvastatin, etc.). A creatinine clearance < 30 ml/min also increases plasma levels of sildenafil. SAFETY PROFILE OF SILDENAFIL: Sildenafil is safe in healthy subjects. In a postmarketing study on 6,527 males, no increase of cardiovascular events was found. However, in older males with coronary heart disease, the risk of sildenafil and the risk of physical exercise during sexual intercourse contribute both to fatal outcomes. Of 69 cases reported to the FDA, 46 patients might have had a cardiovascular event, and in twelve a possible interaction with nitrate use has been reported. Sildenafil is absolutely contraindicated in patients taking long-acting nitrates, those with severe aortic stenosis, and patients with hypertrophic obstructive cardiomyopathy (HOCM). No nitrates should be used within 24 h of sildenafil use. Caution is necessary in patients with a combination of antihypertensive medications, and in patients with cardiac insufficiency. A "pre-Viagra" treadmill test to assess for the presence of stress-induced ischemia can be helpful for both the patient and the physician. If the patient can achieve > or = 5 METs without demonstrating ischemia, the risk of ischemia during coitus is low. MANAGEMENT OF SEVERE ADVERSE EVENTS: If severe hypotension occurs, aggressive fluid resuscitation is the first step, followed by administration of vasoactive drugs and, if necessary, by intraaortic balloon counterpulsation. If unstable angina or myocardial infarctions occurs after the use of sildenafil, the patient is treated according to the guidelines, but without nitrates. CONCLUSION: Sexual activity is a cornerstone of quality of life. However, giving the incidence of "occult" cardiovascular disease in patients with ED and the indications and contraindications of PDE 5 inhibitors in patients with cardiovascular diseases, all patients with ED must be evaluated by a cardiovascular specialist.

Coronary Disease↗

[Cardiogenic shock: pathophysiology, clinics, therapeutical options and perspectives].

Documented mortality from myocardial infarction (MI) has significantly decreased from around 30% in the 1960s to 6-7% currently, following the introduction of intensive care treatment, thrombolysis, effective antithrombotic therapy and coronary angioplasty. However, the approximate mortality of 70-80% of patients with cardiogenic shock following acute MI has hardly improved despite the introduction of modern treatment strategies. The major cause of in-hospital MI mortality remains myocardial failure with consecutive cardiogenic shock and multi-organ failure. Prompt coronary revascularisation by "facilitated" or "adjunctive" percutaneous coronary intervention (PCI), is currently considered the best method to reduce the high mortality in these patients. Facilitated PCI includes administration of glycoproteine receptor antagonists, mechanical circulation support strategies, such as, intraaortic balloon counterpulsation and potentially prehospital thrombolysis.

Angioplasty, Balloon, Coronary↗

[Patients in circulatory shock in emergency and intensive care units].

Patients in circulatory shock are being treated in emergency as well as in intensive care units. Despite different resources in personnel and technical equipment in both areas, patient management has to follow standardized protocols. Diagnosis of shock has to be based upon objective parameters (lactate, pH, standard bicarbonate, arterial blood pressure, central venous pressure, cardiac output). Aim of shock treatment is restoration of adequate tissue perfusion with the use of fluid and red blood cell replacement, vasoconstrictors, inotropics, substances improving microcirculation, and mechanical circulatory support. Target values are: mean arterial blood pressure >80 mmHg, central venous pressure >6 mmHg, hemoglobin >8.0 g/dl, cardiac index >3.5 l/min/m(2). New concepts for optimization of hemodynamics and hematocrit, cortisone, intraaortic balloon counterpulsation, mechanical ventilation with low tidal volumes, and intensive insulin therapy are discussed. However, as shock reversal is dependent on its reason, clarification and treatment of the shock causing event has to be performed with highest priority.

Combined Modality Therapy↗

Successful treatment of severe myocardial failure after postpartum haemorrhage with the use of an intra-aortic balloon pump.

We report a 29-year-old primigravid who developed cardiac failure following postpartum haemorrhage unresponsive to volume resuscitation and therapy with catecholamines and phosphodiesterase-inhibitors. Transoesophageal echocardiography (TEE) demonstrated left atrial and ventricular dilatation and global left ventricular hypokinesis. No elevation of serum MB-isoenzyme fraction was detected and other organ functions remained stable. Although emergency cardiac transplantation was considered in the presented patient, the institution of intra-aortic counterpulsation was decided on as a first treatment option. Intra-aortic balloon counter-pulsation rapidly improved cardiac function and led to weaning from pharmacological cardiac support within a few days. Mechanical circulatory assist devices can be life-saving in postpartum-haemorrhage-associated cardiac failure.

Adult↗

Surgical repair of postinfarction ventricular septal defect: 10-year experience.

Postinfarction ventricular septal defect (PIVSD) remains a surgical challenge resulting in devastating mortality rates. We present our 10-year experience in surgical management of this catastrophic complication of acute myocardial infarction. During a decade (1987-1996) 14 patients with PIVSD were treated surgically in our department. There were 10 men and 4 women, ranging in age from 51 to 78 years. The rupture occurred within the first 4 days after the infarction in most cases (n = 10). Eight patients were supported perioperatively by intraaortic balloon counterpulsation (IABP). In all cases the surgical technique included infarctectomy and ventricular septum reconstruction with synthetic patches. Coronary artery bypass grafting was synchronously performed in four patients. Seven patients died perioperatively (mortality rate 50%) due to heart failure and to multiple organ failure. The most frequent complications were low cardiac output syndrome, hemorrhage, and respiratory and renal insufficiency. The PIVSD needs urgent surgical intervention with the patient hemodynamically stable after cardiac catheterization. Long-term results are favorable for survivors.

Aged↗

[Therapy of acute heart failure, medicamentous strategy].

The leading pathophysiology of acute heart failure and cardiogenic shock is acute or subacute myocardial infarction. Reperfusion of the occluded coronary vessel accompanied by adequate support of cardiac function via assist systems, preferentially the intraaortic balloon counterpulsation, is the therapy of choice. Adjustment of preload (high pulmonary capillary pressure in-acute myocardial infarction with small heart, low pulmonary capillary wedge pressure in patients with large ventricles and chronic heart failure, high central venous pressure in patients with right heart failure, and right ventricle myocardial infarction) and afterload (peripheral arterial vasodilatation, recommended systolic arterial pressure 80-90 mm Hg) but not maximization of cardiac output play an important role. Positive inotropic drugs should be considered when these strategies fail. In acute right heart failure in pulmonary hypertension, a preferential pulmonary vasodilatation with intravenous or inhalative prostaglandins or inhalative NO are of utmost importance. Systemic hypotension is not a contraindication in this pathophysiology.

Cardiotonic Agents↗

Peripartum Cardiomyopathy.

It is critical that the diagnosis of peripartum cardiomyopathy is limited to women with congestive heart failure and decreased systolic function of the left ventricle in last month of pregnancy or within 5 months after delivery. Patients must have no pre-existing cardiac disease and no other cause for current cardiac dysfunction. The inclusion of patients before the last month of pregnancy or after 5 months postpartum introduces a large number of patients with cardiac disorders due to causes other than peripartum cardiomyopathy. Ventricular performance at rest and with exertion determines the type of management, its intensity, and duration. Patients whose ventricular function is normal at rest and with exercise or dobutamine can have their heart failure therapy tapered and ultimately discontinued after 6 to 12 months of standard treatment. Those with normal resting but abnormal stress cardiac function should continue some form of medical therapy (afterload reduction or beta-blocker) for longer periods of time, if not for life. Those with persistently abnormal ventricular function must receive optimal heart failure therapy forever and face the same relatively poor prognosis as patients with dilated cardiomyopathy from any cause. Options for management include standard heart failure therapy (digoxin, diuretics, afterload reduction, and anticoagulation), Swan-Ganz catheter monitoring and use of inotropic agents, intra-aortic balloon counterpulsation, and left ventricular assist device. Patients with peripartum cardiomyopathy are candidates for heart transplantation, assuming they meet all other criteria.

Journal Article↗

Therapeutic Strategies for Cardiogenic Shock.

Cardiogenic shock is a devastating consequence of acute myocardial infarction; it is associated with an extremely high mortality. Treatment strategies should be focused on prompt reperfusion, as well as hemodynamic support. The optimal approach for therapy is emergent angiography and revascularization using percutaneous coronary intervention or coronary artery bypass surgery, with the assistance of intra-aortic balloon pump counterpulsation. Several adjunctive pharmacologic agents, particularly inotropic drugs and vasopressors, are also helpful for hemodynamic support. However, these agents have not been shown to provide a survival benefit, and their use is primarily based on clinical experience.

Journal Article↗

Selection of optimal therapy for chronic stable angina.

Patients with chronic stable angina (CSA) seek a medical opinion for relief of their symptoms and because of fear of having a heart attack. The underlying lesion responsible for CSA is often a severe narrowing of one or more coronary arteries. In addition, the coronary arteries of patients with CSA contain many more nonobstructive lesions, which progress at variable rates, and are prone to rupture and may manifest as acute coronary syndromes (myocardial infarction , unstable angina , or sudden ischemic death). Most patients with CSA can be managed with medical treatment. For angina relief, optimum doses of one of the antianginal drugs (beta blockers , long-acting organic nitrates, or calcium channel blockers ) should be used. If the patient remains symptomatic, combination treatment of BBs plus nitrates or BBs plus dihydropyridine CCBs, or nondihydropyridine CCBs plus nitrates should be tried. Triple therapy has not been shown to be more effective than treatment with two agents. To reduce the incidence of MI, UA, and sudden ischemic death, treatment strategies should include smoking cessation, daily aspirin, daily exercise, and pharmacologic therapy for dyslipidemias, and for elevated blood pressure. Patients who remain symptomatic despite medical therapy and those not willing to take or unable to tolerate antianginal drugs should be considered for percutaneous or surgical coronary revascularization. Patients who do not respond to medical therapy and are not candidates for a revascularization procedure may be considered for additional treatment with trimetazidine or nicorandil (these drugs are not available in the United States or approved by the US Food and Drug Administration, but are available in some other countries). Ranolazine also looks promising but is not yet available for clinical use. As a last resort, enhanced external counterpulsation, spinal cord stimulation, sympathectomy, or direct transmyocardial revascularization should be considered for symptom relief.

Journal Article↗

Therapeutic strategies for cardiogenic shock, 2006.

Cardiogenic shock, a devastating consequence of acute myocardial infarction, is associated with extremely high mortality. Treatment strategies should focus on prompt reperfusion and hemodynamic support. The primary approach for therapy is emergent angiography and revascularization using percutaneous coronary intervention or coronary artery bypass surgery, with the assistance of intra-aortic balloon pump counterpulsation. Several adjunctive pharmacologic agents, particularly inotropic drugs and vasopressors, are also helpful for hemodynamic support. However, these agents have not been shown to provide a survival benefit, and their use is primarily based on clinical experience. Since our last publication, several important advances have been made in the understanding and treatment of cardiogenic shock. Recent evidence suggests that a systemic inflammatory response, including the upregulation of inducible nitric oxide synthase, complement activation, and an inflammatory cytokine cascade, play a role in the development of cardiogenic shock. Newer therapeutic strategies, including C5 inhibitors and nitric oxide synthase inhibitors, are being combined with traditional strategies, such as inotropic agents, vasopressors, and circulatory assist, to treat cardiogenic shock.

Journal Article↗

Acute Pulmonary Edema.

Patients with acute cardiogenic pulmonary edema require rapid assessment and therapy to prevent progression to respiratory failure and cardiovascular collapse. The goal of therapy is to decrease the pulmonary capillary wedge pressure by decreasing intravascular volume and shifting the blood volume into peripheral vascular beds. Mainstays of therapy include morphine sulfate (a venodilator and an anxiolytic), furosemide (a venodilator and diuretic), nitroglycerin preparations (venodilators), and, in some cases, aminophylline, nitroprusside, and beta-adrenergic agents or milrinone. Patients who do not respond to more conservative measures may require interventional procedures, including Swan-Ganz catheterization or arterial pressure monitoring, continuous positive airway pressure or mechanical ventilation, intra- aortic balloon counterpulsation, and mechanical removal of fluid. Because the prognosis for patients with acute cardiogenic pulmonary edema depends on identification and correction of the underlying disease process, it is essential to define the cause of the edema during and after stabilization of the patient. Evaluation should include Doppler echocardiography, cardiac catheterization, and coronary angiography.

Journal Article↗

Clinical transvenous cardioversion of recurrent life-threatening ventricular tachyarrhythmias: low energy synchronized cardioversion of ventricular tachycardia and termination of ventricular fibrillation in patients using a catheter electrode.

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was less than or equal to 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks less than or equal to 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.

Aged↗

Comparative hemodynamic effects of dopamine and dobutamine in patients with acute cardiogenic circulatory collapse.

The hemodynamic effects of dopamine (DPM) and dobutamine (DBM) were compared in 13 patients with acute cardiogenic circulatory collapse. All patients presented with acute pump failure and inadequate systemic perfusion, and most were hypotensive. Nine patients had an acute myocardial infarction (AMI); the other four patients had an acute decompensation of a previously stable ischemic cardiomyopathy, and presented with a low-output syndrome in the absence of documented AMI. Patients were studied with a randomized single crossover design using each patient as his own control. Both drugs were given at doses of 2.5, 5, and 10 micrograms/kg/min for periods of 10 minutes at each dose while hemodynamics were monitored. No other vasoactive drugs were used during the study. Because of advanced age or severe peripheral vascular disease, no patient was considered suitable for intra-aortic balloon counterpulsation. There were no significant differences between the two drugs with regard to heart rate, mean-arterial pressure, systemic vascular resistance, stroke work index, or mean right atrial pressure. DBM improved stroke index and cardiac index significantly (p less than 0.05) more than DPM at doses of 5 micrograms/kg/min. DPM increased left ventricular filling pressure (LVFP) more than DMB at 5 micrograms/kg/min (p less than 0.001) and at 10 micrograms/kg/min (p less than 0.05). Although both DPM and DBM are useful in acute cardiogenic circulatory collapse, there appear to be important differences in their effect on LVFP and in the mechanisms whereby they increase blood pressure.

Acute Disease↗

Risk identification at the time of admission to coronary care unit in patients with suspected myocardial infarction.

The in-hospital clinical course was evaluated in 2,162 consecutive patients admitted with a diagnosis of suspected myocardial infarction. Of these, 1609 patients were considered to be in the high-risk group, based on the presence of 16 clinical criteria present at the time of admission. The remaining 553 patients were classified as low risk. The overall rate of complications in the coronary care unit was greater in the high-risk group, 64%, compared to 26% in the low-risk group (p less than 0.001). Similarly life-threatening events (occurrence or recurrence of ventricular fibrillation, sustained ventricular tachycardia, complete heart block, asystole, or cardiogenic shock) were more common in the high risk-group compared to the low-risk group, 11% and 0.9%, respectively (p less than 0.001). The high-risk group required significantly more interventions, such as electrical cardioversion, temporary pacing, pulmonary artery catheterization, and intraaortic balloon counterpulsation, compared to the low-risk group (20% vs 2%, respectively; p less than 0.001). Myocardial infarction was confirmed in 892 patients in the high-risk group (55%) compared to 90 (16%) in the low-risk group (p less than 0.001). The coronary care unit mortality rate was greater in the high-risk group compared to the low-risk group (8.2% vs 0.4%, respectively; p less than 0.0002). It is concluded that based on readily available clinical criteria at the time of admission, a subgroup of patients at low risk for developing life-threatening complications requiring coronary care unit interventions can be identified and admitted directly to an intermediate-care unit.

Coronary Care Units↗

Coronary and circulatory support strategies for percutaneous transluminal coronary angioplasty in high-risk patients.

PTCA is now applied to patients with unstable acute ischemic syndromes, severe multivessel coronary artery disease, and impaired left ventricular function. To minimize the risk during angioplasty, several coronary and systemic circulation support approaches have been developed as adjuncts to high-risk angioplasty. Local coronary support techniques include the perfusion balloon catheter, the coronary stent, directional coronary atherectomy, laser balloon angioplasty, perfluorocarbon coronary perfusion, coronary sinus retroperfusion, and distal coronary hemoperfusion. Systemic circulatory support includes intraaortic balloon counterpulsation, cardiopulmonary support, the hemopump, and left heart partial bypass. These support devices, while associated with significant complications, may ultimately improve the safety of coronary angioplasty and allow its application to those who would otherwise not be candidates for revascularization.

Angioplasty, Balloon, Coronary↗

Modification of intraaortic balloon catheter to permit introduction by cardiac catheterization techniques.

Intraaortic balloon counterpulsation has been widely applied for treatment of left ventricular pump failure and intractable angina. However, its use has been limited by the difficulty of balloon insertion in some patients and vascular complications in others. An AVCO intraaortic balloon was modified by the addition of a central lumen to allow pressure monitoring, injection of contrast medium and passage of a guide wire. The device was successfully used in 15 of 16 patients, including 4 of 5 in whom attempts to place a standard balloon catheter had failed. No significant vascular complications occurred in any patient. The modified balloon catheter appears to increase the efficacy and safety of insertion and allows immediate and continuous monitoring of arterial pressure.

Adult↗