A simple technique to prevent limb ischemia during veno-arterial ECMO using the femoral artery: the posterior tibial approach.

Lower extremity ischemia is common when the femoral artery is used for veno-arterial extracorporeal membrane oxygenation (VA ECMO). We describe a new technique to reperfuse the extremity. The ipsilateral posterior tibial artery is exposed via a small incision behind the medial malleolus. The vessel is cannulated in a retrograde fashion and connected to the arterial limb of the ECMO circuit. Thirty-six patients received a posterior tibial reperfusion cannula: average flow was 155.8 ml/min and increased over the initial 24 hours. Fifty-eight percent received the posterior tibial cannula within 6 hours of ECMO initiation and none sustained permanent lower extremity injury. Of the remaining 42%, three required amputation or developed permanent neurologic injury. Overall survival was 41%. Cannulation of the posterior tibial artery is a simple technique to reperfuse the lower extremity during VA ECMO. The cannula should be inserted within 6 hours of ECMO initiation to avoid irreversible ischemic damage.

Heart transplantation in the United States, 1999-2008.

This article features 1999-2008 trends in heart transplantation, as seen in data from the Organ Procurement and Transplantation Network (OPTN) and the Scientific Registry of Transplant Recipients (SRTR). Despite a 32% decline in actively listed candidates over the decade, there was a 20% increase from 2007 to 2008. There continues to be an increase in listed candidates diagnosed with congenital heart disease or retransplantation. The proportion of patients listed as Status 1A and 1B continues to increase, with a decrease in Status 2 listings. Waiting list mortality decreased from 2000 through 2007, but increased 18% from 2007 to 2008; despite the increase in waiting list death rates in 2008, waiting list mortality for Status 1A and Status 1B continues to decrease. Recipient numbers have varied by 10% over the past decade, with an increased proportion of transplants performed in infants and patients above 65 years of age. Despite the increase in Status 1A and Status 1B recipients at transplant, posttransplant survival has continued to improve. With the rise in infant candidates for transplantation and their high waiting list mortality, better means of supporting infants in need of transplant and allocation of organs to infant candidates is clearly needed.

Coronary heart disease. Differential hemodynamic, metabolic, and electrocardiographic effects in subjects with and without angina pectoris during atrial pacing.

Right atrial pacing was performed in 41 subjects with coronary heart disease. Twenty developed angina pectoris during pacing, while 21 did not. The extent of coronary artery disease, as judged by selective cinearteriography, was similar in the two groups. Both had significant increases in heart rate and pressure-time per minute, but there was no significant difference in either of these parameters between groups. Among the hemodynamic parameters measured, the only statistically significant change was in the cardiac index which fell slightly but significantly in the angina group. There were no differences in myocardial oxygen extraction either within each group or between groups. In the angina group, however, 14 of 20 subjects exhibited abnormal myocardial lactate metabolism during pacing. The mean change was highly significant (P < 0.01). In the nonangina group, eight of 21 subjects had abnormal lactate metabolism during pacing and the mean change was significant (P < 0.05). There was no correlation between abnormal lactate metabolism and electrocardiographic evidence of myocardial ischemia in either group. Sublingual nitroglycerin, given to five subjects with angina while pacing was continued, resulted in prompt relief of symptoms, but abnormal lactate metabolism and ST-segment depression were unaffected after 10 min. By contrast, when anginal symptoms were relieved in five subjects by cessation of pacing, symptomatic improvement was accompanied by marked improvement in lactate metabolism after 10 min. Although angina pectoris appears to be related statistically to subnormal left ventricular function and abnormal lactate metabolism, there is significant individual variation.

Coronary angiographic morphology in myocardial infarction: a link between the pathogenesis of unstable angina and myocardial infarction.

It has previously been shown that analysis of coronary morphology can separate unstable from stable angina. An eccentric stenosis with a narrow neck or irregular borders, or both, is very common in patients who present with acute unstable angina, whereas it is rare in patients with stable angina. To extend these observations to myocardial infarction, the coronary morphology of 41 patients with acute or recent infarction and nontotally occluded infarct vessels was studied. For all patients, 27 (66%) of 41 infarct vessels contained this eccentric narrowing, whereas only 2 (11%) of 18 noninfarct vessels with narrowing of 50 to less than 100% had this lesion (p less than 0.001). In addition, a separate group of patients with acute myocardial infarction who underwent intracoronary streptokinase infusion were also analyzed in similar fashion. Fourteen (61%) of 23 infarct vessels contained this lesion after streptokinase infusion compared with 1 (9%) of 11 noninfarct vessels with narrowing of 50 to less than 100% (p less than 0.01). Therefore, an eccentric coronary stenosis with a narrow neck or irregular borders, or both, is the most common morphologic feature on angiography in both acute and recent infarction as well as unstable angina. This lesion probably represents either a disrupted atherosclerotic plaque or a partially occlusive or lysed thrombus, or both. The predominance of this morphology in both unstable angina and acute infarction suggests a possible link between these two conditions. Unstable angina and myocardial infarction may form a continuous spectrum with the clinical outcome dependent on the subsequent change in coronary supply relative to myocardial demand.

Treatment of atrial arrhythmias. Effectiveness of verapamil when preceded by calcium infusion.

Intravenous verapamil hydrochloride was used alone in 63 episodes of atrial fibrillation and flutter and six episodes of supraventricular tachycardia (SVT) (group A). Calcium chloride was given intravenously prior to verapamil in 41 episodes of fibrillation and flutter and 18 episodes of SVT (group B). All patients with SVT converted to normal sinus rhythm, with eight in group B converting after administration of calcium alone. Therapy lowered the heart rate in all patients with fibrillation and flutter; however, those given verapamil alone had a mean decrease in systolic pressure of 18.8 mm Hg; there was no change in those pretreated with calcium. The mean dose of verapamil required by group B was significantly lower than in group A. Many with atrial fibrillation or flutter who received digoxin subsequently converted to sinus rhythm. Thus, pretreatment with calcium decreased the hypotensive effect of verapamil without compromising its antiarrhythmic effect.

Heparin resistance induced by intravenous nitroglycerin. A word of caution when both drugs are used concomitantly.

Intravenous (IV) nitroglycerin was found to interfere with the anticoagulant effect of heparin during eight infusions of both drugs in seven patients who were closely monitored with frequent activated partial thromboplastin time determinations. All patients were resistant to heparin when receiving IV nitroglycerin and had a marked increase in sensitivity when discontinuing the IV nitroglycerin therapy. This effect was present whether or not propylene glycol was in the preparation. Patients treated with simultaneous IV nitroglycerin and IV heparin must be monitored often to avoid inadequate anticoagulation, and heparin dosage should be decreased when stopping IV nitroglycerin therapy to avoid hemorrhage.

Chewing nifedipine to rapidly treat hypertension.

Nifedipine, a calcium channel-blocking agent, was administered buccally to 63 patients who had a diastolic BP of 120 mm Hg or higher (51 patients) or a systolic BP of 200 mm Hg or higher (46 patients). Forty-two patients responded to one dose of 10 mg of nifedipine with a drop in BP from 205.5 +/- 24.4/127.7 +/- 11.7 (mean systolic BP +/- SD/mean diastolic BP +/- SD) to 158.6 +/- 24.7/88.8 +/- 10 mm Hg in 39.9 +/- 13.0 minutes (mean +/- SD). Nineteen patients responded to two doses of 10 mg of nifedipine with a drop in BP from 212.1 +/- 27.1/128.2 +/- 17.3 to 165.4 +/- 24.5/93.8 +/- 10.7 mm Hg after 66.0 +/- 17.8 minutes. There were no side effects and no hypotension even among the 38 patients who had recently received other medications. Chewing perforated nifedipine capsules is a safe and effective method to lower BP promptly without parenteral medications.

The value of tilt table testing with isoproterenol in determining therapy in adults with syncope and presyncope of unexplained origin.

BACKGROUND: Previous studies have shown the effectiveness of tilt table testing in establishing the diagnosis of neurocardiogenic syncope and in dictating therapy in patients with syncope of unknown origin. Most studies have been limited by small numbers of patients and brief follow-up. Tilt table testing was performed with and without isoproterenol hydrochloride in 94 patients, and therapy was determined by the test findings. The patients were followed up for at least 10 months (mean, 17.8 months). METHODS: The 80 degrees tilt table test was performed in 94 consecutive patients who presented with syncope (n = 74) or presyncope (n = 20) and in whom neurologic and cardiac causes were ruled out. Therapy was determined by the tilt test findings. Sixty-seven patients were followed up for 17.8 +/- 5.3 months (mean +/- SD) (range, 10 to 27 months). RESULTS: Forty-nine patients had positive results of tilt studies and received therapy. Of these 49 patients, 36 returned for second tilt studies while they were taking medication, and 30 had negative results. Six patients had medication changes and had negative results of follow-up tilt studies. No symptoms were noted on follow-up in the 24 patients who presented with syncope and who had positive results of tilt tests that responded to therapy. Of these 35 patients presenting with syncope who had negative results of initial tilt studies and who did not receive any therapy, syncope recurred in four patients. Three of 10 patients contacted who presented with presyncope and had negative results of tilt studies reported symptoms. CONCLUSIONS: Tilt table testing is an excellent tool for diagnosing neurocardiogenic syncope in adults and in determining effective therapy in patients presenting with syncope of unknown origin.

Computed tomography of the abdomen in the diagnosis of splenic emboli.

Abdominal computed tomographic scans were performed in 25 consecutive patients with bacterial endocarditis. Six patients had splenic infarcts, only two of whom had symptoms. Three of the six patients had no evidence of emboli to other organs. In patients with endocarditis who have had clinically apparent emboli or who are, for other reasons, being considered for valvular surgery, a computed tomographic scan of the abdomen may help in decision making.

Effects of lignocaine on intramyocardial conduction in nonischaemic and ischaemic canine myocardium.

The effect of lignocaine (USP: lidocaine) on intramyocardial conduction in ischaemic and nonischaemic areas of the left ventricular myocardium was determined in 11 mongrel dogs. Intramyocardial conduction times were assessed during control conditions, 15 min after coronary ligation, and following lignocaine administration. Coronary occlusion resulted in a disparity between the conduction velocities in the ischaemic and nonischaemic zones. Ater lignocaine administration conduction to the ischaemic area was further decreased. However, conduction to the nonischaemic area was decreased to a relatively greater extent, resulting in a significant decrease in the disparity of conduction velocities in the two areas. It is concluded (1) that lignocaine exerts dissimilar quantitative effects on the nonischaemic and acutely ischaemic myocardium and (2) that these differential effects decrease the inhomogeneity of intraventricular conduction. It is possible that this action may play a role in the suppression of re-entrant arrhythmias.

Electrophoretic patterns of proteins in cystic fibrosis sweat.

The abnormal gene product in cystic fibrosis has not been identified. We report that two-dimensional polyacrylamide gel electrophoresis of 125I-labeled sweat proteins coupled with fluorography and rare earth screen radioautography reveals an absence of an acidic protein of molecular weight 60,000 in sweat collected from 9 patients with cystic fibrosis. The protein spot was present in sweat from heterozygotes and from controls.

Role of blood platelets in coronary artery disease.

Over the past decade, research in blood platelet physiology has led to the suggestion that platelets play an important part in the pathogenesis and complications of coronary artery disease. Occlusive intravascular platelet aggregates have been shown to cause ischemic myocardial damage in the experimental animal and to be present in some patients who die suddenly. The interplay between endothelial damage and platelet aggregation has been implicated in the etiology of atherosclerosis. Products released from platelets during aggregation may cause arterial spasm. Patients with overt ischemic heart disease and with the risk factors associated with coronary artery disease have been found to have abnormally reactive platelets. Clinical studies of drugs that inhibit platelet aggregation have been reported to show a beneficial effect in preventing cardiac deaths or myocardial infarction; other studies have been negative or shown only a trend toward benefit. This report reviews the theoretical and experimental basis for the platelet hypothesis and the current data on the use of antiplatelet drugs in patients with coronary disease.

Coronary arteriographic findings in symptomatic right bundle branch block.

Of 5,132 consecutive patients who had coronary arteriography for chest pain, 103 (2%) had right bundle branch block (RBBB), 66 (64%) of whom had no electrocardiographic evidence of concomitant myocardial infarction (MI); 23 patients had evidence of MI of the inferior wall, 8 of the anterior wall and 6 of the lateral wall. The incidence, location or severity of coronary artery disease (CAD) in patients with RBBB alone were not significantly different from those in 110 similarly symptomatic patients with normal ECGs. However, significantly more left ventricular contraction abnormalities, especially in the anteroapical area, were found in patients with RBBB (p less than 0.01). Similarly, patients with RBBB and inferior MI, compared with 60 similarly symptomatic patients with inferior MI without RBBB, showed no significant differences in location, incidence or severity of CAD. However, more left ventricular contraction abnormalities in the apical area were found in patients with RBBB (p less than 0.025). Thus, the presence of RBBB does not suggest more severe or extensive CAD; however, RBBB does predict more left ventricular contraction abnormalities.

Comparison of platelet activation in unstable and stable angina pectoris and correlation with coronary angiographic findings.

We sought to investigate the relation between platelet activation and the angiographic evidence of ruptured plaque in patients presenting with unstable and stable angina pectoris. We prospectively enrolled 25 consecutive patients (5 women and 20 men, mean age 62 +/- 3 years), 17 with unstable angina and 8 with stable angina. Systemic venous blood samples were collected within 4 to 6 hours of admission for flow cytometry analysis. Activation-dependent epitope CD63 and glycoprotein IIb/IIIa on the platelet membrane were assayed. Fibrinogen levels were also measured. All patients with unstable angina underwent cardiac catheterization and had angiographic evidence of ruptured plaque. Of the patients with stable angina, 5 underwent coronary angiography with smooth noncomplex lesions and 3 had negative technetium-99m sestamibi stress tests. Patients with unstable angina were characterized by 39% higher levels of fibrinogen than patients with stable angina (423 +/- 304 vs 304 +/- 51 mg/dl, p = 0.004). The percentage of platelets positive for the activation-dependent epitope CD63 was 5 times higher in patients with unstable than stable angina (14.6 +/- 5.6% vs 2.75 +/- 1.6%, p = 0.0026). They also had a 15% higher expression of their glycoprotein IIb/IIIa (517 +/- 79 vs 449 +/- 50 mean fluorescence intensity, p = 0.038). Thus, this study establishes a direct relation between the morphology of ruptured plaque and platelet activation in patients with unstable angina. This may allow for further risk stratification. Patients with unstable complex lesions had a fivefold higher expression of the platelet activation epitope CD63 than patients with stable angina. Furthermore, they had 15% more glycoprotein IIb/IIIa aggregation sites expressed on their platelet membrane, thus indicating an intense thrombogenic potential.

Wolff-Parkinson-White syndrome type B with His depolarization occurring after the QRS. Further evidence that WPW-QRS is a fusion beat.

His bundle electrograms were recorded in a patient with Wolff-Parkinson-White syndrome (type B) during atrial pacing studies and during the induction of premature atrial depolarization at varying coupling intervals. Early ventricular depolarization (preexcitation) occurred simultaneously with the His depolarization, suggesting that conduction occurred via both the Kent and the normal A-V nodal-His-Purkinje pathway during sinus rhythm. Atrial pacing at increasing rates showed progressive advance of the His spike into the QRS and increasing duration of the delta wave until the appearance of broad bizarre QRS complexes with prolonged P-J intervals, suggesting major, if not total, depolarization of the ventricle by the Kent pathway. PAD's induced at coupling intervals of 360, 330, and 300 msec caused progressive delay of the His bundle depolarization, with the His spike occurring after the QRS at S(1)-H intervals of 230, 265, and 325 msec, respectively, and Q-H intervals of 123, 160 and 220 msec, respectively. These findings suggest that during sinus rhythm the QRS was a fusion beat. With early premature atrial stimulation, conduction occurred solely via the Kent pathway, with conduction via the normal A-V nodal pathway encountering increasing delay. The finding of His depolarization occurring after the QRS suggests retrograde myocardial-His block, and may explain the absence of paroxysmal supraventricular tachycardias in this patient.

Severe coronary artery disease in a marathon runner.

A 55-year-old male runner was found to have severe three-vessel coronary disease on angiography soon after completing a 25-mile marathon with no symptoms. This patient raises important questions concerning our understanding of ischemic heart disease.

Characteristic pulsed Doppler findings in patients with flail mitral valve.

Pulsed mode Doppler findings in the left atrium were studied in 18 patients with moderate to severe catheterization-proven mitral regurgitation, four with and 14 without flail mitral valve. Atypical markedly turbulent antegrade flow in the left atrium was observed in all four patients with flail mitral valve, whereas the typical retrograde mitral regurgitation pattern of flow was observed in the 14 patients without flail mitral valve. This Doppler pattern appears to be indicative of a flail mitral valve.

Evidence suggesting dual A-V nodal pathways in patients without supraventricular tachycardias.

Electrophysiologic evidence for dual pathways of conduction through the A-V node is presented in three patients without history of supraventricular tachycardia. In case 1, abrupt spontaneous changes in the PR interval from 0.17 to 0.42 second were seen. His bundle electrographic studies showed two sets of A-H intervals during sinus rhythm and at several atrial pacing rates, although at rates over 100 per minute only the slow pathway conducted. Using the extrastimulus method, different refractory periods for the fast and slow pathways were documented. Cases 2 and 3 underwent His bundle electrography studies to evaluate intraventricular conduction defects. During atrial pacing studies abrupt changes in the A-H interval, from 220 to 470 msec and from 220 to 370 msec, were observed on increasing the pacing rate from 90 to 95 per minute in case 2 and from 120 to 130 per minute in case 3. In these two patients, dual A-V nodal pathways were suggested by the sudden changes in the A-H -interval at critical pacing rates. These findings indicate that evidence suggesting dual pathways of conduction through the A-V node may not be an uncommon finding and may be present without the manifestation of recurrent supraventricular tachycardias.

Effect of emotional stress on platelet aggregation in humans.

In 16 young house physicians, each of whom presented a case at grand rounds, the effect on platelet function of the emotional stress involved in presenting the case was determined. Platelet-aggregation curves, using adenosine diphosphate and epinephrine, were determined immediately before, immediately after, and seven days after stress. Platelet aggregation was diminished during the stress period in 15 of the subjects. These findings may possibly be of importance in the relationship between stress and myocardial infarction; they also suggest that the emotional state of the patient must be considered when interpreting platelet-aggregation curves.

Use of tissue plasminogen activator in the coronary care unit for acute closure after coronary angioplasty.

Coronary angioplasty in a patient ten days following myocardial infarction was complicated by repeated thrombotic occlusion requiring intracoronary streptokinase. Recurrence of chest pain and ST elevations after transfer to the coronary care unit was successfully managed with intravenous tissue plasminogen activator without returning the patient to the catheterization laboratory.