Complications of cardiac catheterization in the current era: a single-center experience.

Consecutive cardiac catheterization procedures done over a 2-yr period (April 1996 to March 1998) were prospectively analyzed to determine and characterize procedure-related complications (in-hospital and 1-mo follow-up), as they occur at present. During the study period, 11,821 procedures (7,953 diagnostic and 3,868 therapeutic) were performed. The majority of procedures (> 60%) were done in high-risk patients. Stents were implanted in 33% of patients, and adjunctive abciximab was used in 6.6% of therapeutic procedures. The overall complication rate was 8% (3.6% of diagnostic procedures and 15.1% of therapeutic procedures). The procedure-related mortality rates were 0.2%, 0.1%, and 0.5% for total, diagnostic, and therapeutic procedures, respectively. Cardiac complications were seen in 3.9% (1.5% of diagnostic and 9% of therapeutic procedures). Emergency cardiac surgery was required in 0.05% of the diagnostic procedure group and 0.3% of the therapeutic procedure group (total, 0.1%). Despite marked changes in patient population and practice, the complication rates of cardiac catheterization remain very low.

Intravascular ultrasound for diagnosis of left main coronary artery stenosis.

Coronary angiography has many limitations for the assessment of coronary artery disease. Intracoronary ultrasound imaging may overcome some of these limitations by providing direct visualization of the luminal area. This report describes a case where intracoronary ultrasound imaging was useful for correct assessment of left main coronary artery disease which enabled avoidance of coronary artery bypass grafting in this patient. Intravascular ultrasound may be a good complement to coronary angiography in selected cases of left main coronary artery lesion.

The effects of stress, emotion, and behavior on the heart.

The relationships between emotional status, neurohormonal control and the cardiovascular function are reviewed. In the first part of this paper, we reviewed (1) the pathways between brain and heart, physiology of the defense reaction and the role of the autonomic nervous system in the mediation of the effects of stress; (2) the cardiac manifestations of emotional stress, and (3) the role of stress and the influence of circadian variations in the occurrence and development of myocardial ischemia, myocardial infarction and sudden death. In the second part, we discussed the relationship between behavior, coronary heart disease and particularly the role of the so-called type A behavior and hostility. Finally, we emphasize the importance of life-style changes to improve the prognosis of coronary disease and to limit the progression and ultimately to cause a regression of atherosclerosis. Thus, it appears that a transdisciplinary approach associating cardiologists, neuroscientists and behavior scientists will help to devise more effective strategies for the prevention and early therapy of cardiovascular disease.

Apical hypertrophic cardiomyopathy: clinical and angiographic characteristics of the first Canadian series.

Originally described in Japan, 'apical hypertrophic cardiomyopathy' has now been reported in many other countries. A series of eight patients who present with the classic 'spade-like' left ventricular angiographic pattern are reported; five of them also had hypertension. Thus, this angiographic pattern may not be specific for apical hypertrophic cardiomyopathy and may be seen in acquired heart disease.

Vascular bed and vasoconstrictor-dependent selectivity of the calcium channel antagonist, PN 200-110.

The potency of the dihydropyridine calcium channel blocker, PN 200-110 was assessed in vitro against contractions induced by potassium (20-55 mM) and histamine (1-300 microM) in rabbit thoracic aorta, coronary, basilar, renal and central ear arteries. PN 200-110 was particularly effective against potassium responses in the coronary and basilar arteries (IC50 30 and 50 pM) and of little effect against histamine responses in the renal artery and thoracic aorta (IC50 greater than 1 microM). These results suggest that PN 200-110 has some preferential actions dependent on both the vascular bed and also the constrictor used.

Atrial natriuretic factor: a possible link between left atrium, plasma volume, adrenergic control and renin-aldosterone in the mitral valve prolapse syndrome.

The immunoreactive atrial natriuretic factor (ANF) was measured by radioimmunoassay after extraction with SEP-PAK cartridges in 16 hyperadrenergic patients with the mitral valve prolapse (MVP) syndrome. Plasma renin activity and plasma aldosterone were concomitantly measured by radio-immunoassay. Plasma and blood volumes were obtained indirectly after measurement of red cell volume. Norepinephrine and epinephrine were measured by a radio-enzymatic microtechnique. Seven out of 16 patients (44%) had high values of immunoreactive ANF. Blood volume was uniformly decreased in MVP patients, but this was more marked in patients with high ANF. There was a significant correlation between ANF and the reduction in blood volume. Plasma norepinephrine was not significantly different in patients with high ANF and low or normal ANF. Thus, some patients with the MVP syndrome may have both an increased adrenergic state and abnormal values of ANF. The interplay between these two neuro-endocrine disorders may account for some of the symptoms of these patients. The data confirm that this syndrome may be associated with a complex 'neuro-endocrine cardiovascular process'.

[Evaluation of new pericardial bioprostheses by pulsed and continuous Doppler ultrasound ]. / Evaluation des nouvelles bioprothèses péricardiques par Doppler pulsé et continu.

The authors have studied by pulsed and continuous Doppler ultrasonography 108 pericardial prostheses in a good functional state implanted for less than five years to patients without any clinical and echographic signs of heart failure. The pulsed Doppler ultrasonography allowed to exclude the possible dysfunction of the prostheses; continuous Doppler ultrasonography allowed the measurement of the maximal transprosthetic velocities and to deduce the corresponding maximal and middle gradients by means of simplified Bernouilli's equation. Using three types of bioprostheses (Carpentier-Edwards, Ionescu and Mitroflow) the following problems were investigated: Normal ranges of maximal transprosthetic velocity and gradients. At the aortic level the maximal velocity ranges from 1.60 to 2.83 +/- 14 m/s and the maximal gradients from 10 for size 27-29 to 32 +/- 3.3 mmHg for size 19. At the mitral level the maximal velocity ranges from 0.80 to 2 m/s and the mean gradients from 1 for size 33 to 7 mmHg for size 25. The mean half-life of decrease is 100 +/- 28 ms. Thus all aortic bioprostheses appear to be stenosing, which is not the case for the mitral ones, size 31 and 33. Factors governing the maximal transprosthetic velocity and the gradients: these determining factors are the size, the type and the age of the bioprosthesis (r = 0.59 for the correlation between maximal velocity and size, r = 0.53 between size and mean aortic gradient). The accessory factors are the age and the functional condition of the myocardium. All these factors have to be considered and neutralized for allowing a valid comparison of various types of prostheses. Comparison of the three pericardial prostheses studied: in patients without signs of myocardial dysfunction of prosthetic origin and with comparable basal conditions, comparison of maximal velocity and of the gradient points to a significant superiority of the Mitroflow at the aortic level and of the Ionescu and Mitroflow at the mitral level. It should be noted in the end that the great similarity of the results obtained in the present study by Doppler ultrasonography with the previously reported hemodynamic data confirms the important role of the Doppler method in the evaluation of valvular bioprostheses.

Prognostic significance of progression of coronary artery disease.

Angiographically documented coronary artery disease (CAD) can progress. Although progression itself is frequently recognized in patients who have undergone repeat cardiac catheterization, its prognostic significance remains unclear. To evaluate the influence of progression on survival, 313 patients with CAD who underwent catheterization twice (39 +/- 25 months apart) were followed for 3 to 129 months (mean 41 +/- 30) after the second angiogram. At the time of the second angiogram, 21, 91, 113 and 88 patients had 0-, 1-, 2- and 3-vessel CAD, respectively. The mean ejection fraction (EF) of the group was 55 +/- 13%. Progression was noted in 139 patients (44%). Of the 313 patients, 33 died and 39 had acute myocardial infarction (AMI) during follow-up. Four-year survival was estimated at 94% and 83% in the nonprogression and progression groups, respectively. Progression was predictive of survival by (univariate) long-rank test (p less than 0.01), but only EF (p less than 0.001), number of diseased vessels (p less than 0.01) and percent stenosis in the left main coronary artery (p less than 0.05) were independently significant by (multivariate) Cox regression analysis. Four-year survival without AMI was 89% and 73% in the nonprogression and progression groups, respectively. Progression was related to survival without AMI (p less than 0.001) by log-rank test. Cox regression analysis provided 3 independent predictors of survival without AMI: number of diseased vessels (p less than 0.01), progression (p less than 0.01), relative risk = 2.28) and EF (p less than 0.01). Results were similar when analyzing only the 39 AMIs.(ABSTRACT TRUNCATED AT 250 WORDS)

Improved exercise tolerance after propranolol, diltiazem or nifedipine in angina pectoris: comparison at 1, 3 and 8 hours and correlation with plasma drug concentration.

Exercise tolerance 1, 3 and 8 hours after 80 mg of propranolol, 120 mg of diltiazem and 20 mg of nifedipine, and after 20 minutes of 0.6 mg of sublingual nitroglycerin were compared with placebo in 15 men who had chronic stable angina pectoris. Three hours after drug ingestion, the exercise time was prolonged by 72 +/- 26, 162 +/- 27 and 161 +/- 30 seconds (p less than 0.05) for propranolol, diltiazem and nifedipine, respectively, and by 123 +/- 35 seconds (p less than 0.001) 20 minutes after sublingual nitroglycerin compared with placebo. The onset of ST-segment depression greater than or equal to 0.1 mV was delayed by 120 +/- 34, 203 +/- 29 and 189 +/- 35 seconds (p less than 0.05) and by 79 +/- 23 seconds (p less than 0.05), respectively. After propranolol, the peak rate-pressure product decreased compared with placebo (15.1 +/- 1.1 U [10(-3)] vs 20.0 +/- 1.5 U, p less than 0.01). In contrast, the peak rate-pressure product was greater after diltiazem and nifedipine than after placebo (22.2 +/- 1.3 U [p less than 0.05] and 23.8 +/- 1.4 U [p less than 0.01]). The maximal increase in exercise tolerance was most marked for each drug at 3 hours, but was also significant at 1 hour for nifedipine and at 8 hours for diltiazem. At 3 hours, an increase in exercise time of more than 2 minutes was observed in 4 of 6 patients who had plasma propranolol concentrations greater than 40 ng/ml, 8 of 9 who had a plasma diltiazem concentration greater than 150 ng/ml, and in 7 of 7 who had a plasma nifedipine concentration greater than 90 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

QT interval prolongation and increased plasma catecholamine levels in patients with mitral valve prolapse.

The heart rate corrected QT interval (QTc) and plasma catecholamine (CA) and norepinephrine (NE) levels were measured in 15 symptomatic patients with idiopathic mitral valve prolapse (MVP) and in 19 control subjects. MVP patients showed longer mean QTc and were divided into two groups: group A normal QTc (greater than 440 msec) and group B prolonged QTc (less than 440 msec). In supine resting conditions CA levels were as follows: group A 0.420 +/- 0.035 ng/ml and group B 0.619 +/- 0.104 ng/ml (p less than 0.05); both were greater than control values (0.348 +/- 0.017 ng/ml, p less than 0.005). NE levels were as follows: group A 0.350 +/- 0.031 ng/ml and group B 0.376 +/- 0.052 ng/ml (NS); both were greater than control values (0.242 +/- 0.025 ng/ml, (p less than 0.05). When a standing position was assumed, CA and NE levels increased significantly in all groups but this was most marked in group B as compared to control levels (CA: 1.039 +/- 0.123 ng/ml versus 0.625 +/- 0.037 ng/ml; NE: 0.737 +/- 0.076 ng/ml versus 0.504 +/- 0.031 ng/ml) (p less than 0.001 and p less than 0.05, respectively). Thus the longest QTc was observed in patients with MVP who had the highest levels of CA and NE, in both supine and standing positions. These data may account, in part, for the occurrence of severe ventricular arrhythmias in some patients with MVP and may offer a rationale for adrenergic blockade in that subset of patients with MVP and markedly prolonged QTc.

Increased plasma catecholamine levels in patients with symptomatic mitral valve prolapse.

Total plasma catecholamine levels, plasma norepinephrine levels, heart rate, and systolic and diastolic pressures were measured in 15 symptomatic patients with mitral valve prolapse and in 19 normal subjects in supine baseline conditions and in a standing position. In the 15 symptomatic patients, total plasma catecholamine levels and plasma norepinephrine levels were significantly elevated in both positions, and heart rate was lower than in normal subjects in the supine position but returned to normal in the upright position. Thus, symptomatic patients with mitral valve prolapse demonstrate increased resting sympathetic tone. In addition, the associated supine bradycardia suggested that increased vagal tone might also be present at rest. These observations support the hypothesis of a dual autonomic dysfunction in these patients and could account for some of the clinical manifestations of the mitral valve prolapse syndrome.

Increased exercise tolerance and reduced electrocardiographic ischemia with diltiazem in patients with stable angina pectoris.

Diltiazem is a calcium slow-channel blocking drug that may be effective in the treatment of chronic stable angina pectoris. To evaluate the therapeutic efficacy 3 hours after a single oral dose of 120 mg, 12 men with chronic stable angina pectoris performed a maximal exercise test on a bicycle ergometer after ingesting either placebo or diltiazem administered in a double-blind fashion. During submaximal exercise at a fixed work load, diltiazem decreased the average heart rate response from 119 +/- 17 to 107 +/- 14 beats/min (p less than 0.01), systolic blood pressure from 182 +/- 15 to 175 +/- 15 mm Hg (p less than 0.05) and the rate-pressure product from 21.8 +/- 4.2 to 18.8 +/- 3.2 x 10(-3) units (p less than 0.01). The average submaximal work load at which significant ST-segment depression (0.1 mV) first appeared was increased from 355 +/- 142 to 525 +/- 143 seconds (p less than 0.01) after diltiazem. At peak exercise after diltiazem, the average depth of ST-segment depression in any one lead and the extent of myocardial ischemia observed in all 12 ECG leads were decreased (p less than 0.01), even though the average work load was increased by 29% (p less than 0.01). Peak heart rate, systolic blood pressure and rate-pressure product were similar with placebo and diltiazem. The plasma diltiazem concentration was 13.9 +/- 29 ng/ml 3 hours after ingestion and was significantly (p less than 0.05) related to the increased time to the onset of important ST-segment depression (r = 0.65) and to the decrease in the extent of myocardial ischemia observed in all 12 ECG leads (r = -0.61) compared with placebo. Thus, diltiazem is effective in treating chronic stable angina pectoris. It decreases myocardial oxygen requirements during upright exercise and appears to increase myocardial oxygen delivery.

Increased plasma catecholamines in patients with Friedreich's ataxia.

We studied free plasma catecholamines in 23 patients with Friedreich's ataxia, having a mean age of 22 +/- 9.6 (SD) years. Conjugated catecholamines were also studied in 10 patients. Mean plasma norepinephrine and epinephrine were significantly higher than controls both in the supine and standing positions. In total 15 out of 23 patients (65%) had increase free and/or conjugated plasma catecholamines. The increased in plasma catecholamines was more marked in patients with severe neuromotor impairment. Among the patients with left ventricular concentric hypertrophy (wall thickness greater than 12 mm), only 3 had no demonstrable sympathetic hyperfunction. Since the high local concentrations of norepinephrine at the site of release from sympathetic nerve terminals may serve as a trigger for the hypertrophic response of the myocardial cell, it is suggested that early pharmacological intervention could prevent or limit the cardiomyopathic process or its clinical consequences.

Pathophysiology of chest pain in patients with cardiomyopathies and normal coronary arteries.

To clarify the pathogenesis of chest pain in patients with cardiomyopathies, we compared coronary blood flow and other indicators of ischemia at rest and during pacing-induced tachycardia in nine patients with cardiomyopathy (four hypertrophic and five congestive) and in five control subjects. Coronary blood flow was reduced at rest and during pacing in cardiomyopathy patients compared with controls. In patients with hypertrophic cardiomyopathy, pacing induced chest pain in all, increased ST-segment depression in three patients and increased coronary venous lactate concentration. With pacing, two of five patients with congestive cardiomyopathy had chest discomfort and three had increased ST-segment depression, but coronary venous lactate concentration did not change significantly. In both groups of cardiomyopathies, the ratio of the systolic and diastolic pressure-time indexes tended to decrease more than in controls during pacing. Thus, myocardial perfusion is decreased in patients with cardiomyopathy, both at rest and during pacing. The changes detected during pacing point to subendocardial ischemia as the likely mechanism for angina in hypertrophic and possibly also in congestive cardiomyopathy.

Predictive value of the ear-crease sign in coronary artery disease.

The value of the ear-crease sign in predicting the presence of coronary artery disease was studied in 340 consecutive patients who underwent coronary arteriography. In this selected population, 75.6% of whom had coronary artery disease, the sensitivity of the sign was 59.5%, the specificity 81.9% and the positive predictive value 91.1%. The sign was associated with increasing age but was also independently associated with obstructive coronary artery disease. No significant correlation was found between the sign and the presence of risk factors or other signs of such disease, except for corneal arcus. In symptomatic patients the sign suggested the presence of more extensive coronary artery disease. In an asymptomatic population with a low prevalence of coronary artery disease it appears to be of limited value in predicting obstructive coronary artery disease. However, it may identify a subset of patients prone to early ageing and to the early development of coronary artery disease, whose prognosis might be improved by early preventive measures.