Improved left ventricular filling accompanies reduced left ventricular mass during therapy of essential hypertension.

Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.

Does the type of venous drainage or cardioplegia affect postoperative conduction and atrial arrhythmias?

Five consecutive patient groups undergoing coronary bypass surgery were studied for postoperative conduction disturbances and atrial arrhythmias. Group I (50 patients) had blood cardioplegic solution (25 meq/liter potassium) and unsnared venae cavae, group II (156 patients) had low-volume crystalloid cardioplegic solution (25 meq/liter potassium) and unsnared venae cavae, group III (56 patients) was similar to group II except that a single cavoatrial venous cannula was used instead of two separate cannulas, group IV (218 patients) had high-volume crystalloid cardioplegic solution (25 meq/liter potassium) and snared venae cavae, and group V (37 patients) was the same as group IV except that the cardioplegic solution contained 10 meq/liter potassium after the first dose, which contained 25 meq/liter. All postoperative electrocardiograms were analyzed for conduction disturbances and atrial arrhythmias. The results showed a significantly lower incidence of conduction disturbances in group I (12%) as compared with groups II to IV. In addition, groups IV and V (high-volume crystalloid cardioplegic solution) had a significantly higher incidence of conduction disturbances than groups II and III (lower-volume crystalloid solution) (55.0% and 62.1% vs 26.2% and 35.1%, respectively). The majority of these disturbances were temporary. Group I also had the lowest incidence of postoperative atrial arrhythmias (3.8%). There was no significant difference between the groups receiving high- and low-volume crystalloid solution. It is concluded that blood cardioplegic solution affords the best protection against postoperative conduction disturbances and atrial arrhythmias. High-volume crystalloid cardioplegic solution affords the least protection against conduction disturbances but has no effect on atrial arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chronic nitrendipine on casual (office) and 24-hour ambulatory blood pressure.

To assess the clinical efficacy of chronic nitrendipine therapy in mild to moderate essential hypertension, we studied blood pressure (BP) and heart rate responses in 22 subjects receiving maintenance nitrendipine therapy. Ten subjects (45%) whose hypertension was controlled with chronic monotherapy had an 11/12 mm Hg decrease in supine BP (P less than 0.05) with a mean (+/- SD) dose of 71 +/- 15 mg/day. The 12 (55%) subjects whose hypertension was not controlled with monotherapy had a comparatively higher baseline BP than the other 10 (156/105 +/- 10/6 compared with 150/98 +/- 15/4 mm Hg; P less than 0.05). Eight of the 10 subjects demonstrating office BP control with chronic nitrendipine monotherapy who also had full-time employment underwent continuous ambulatory BP monitoring before and after maintenance monotherapy. Nitrendipine induced a reduction in the mean 24-hour BP and mean BP at home, but did not reduce the BP during work or while asleep. These data suggest that nitrendipine lowers BP when assessed by casual office methods. The ambulatory BP monitor data demonstrate that the hypotensive response to chronic nitrendipine is modified during work periods, which are generally associated with increased adrenergic activity. Ambulatory BP monitoring may be superior to office (casual) monitoring in the assessment of the overall efficacy of antihypertensive drugs.

Sinus bradycardia associated with peripheral lipids and total parenteral nutrition.

This case report describes a 23-yr-old woman with Crohn's disease who developed sinus bradycardia 4 hr after initiation of total parenteral nutrition with lipids through a peripheral vein. The bradycardia persisted for 1 wk, with only slight improvement when the lipids were held for two 4-hr periods. The heart rate began to improve when lipids were changed from 10 to 20%, and continued to rise after Synthroid was started. The possible relationships between nutritional and thyroid status, as well as lipids and heart rate are discussed.

Rapid ventricular filling in left ventricular hypertrophy: II. Pathologic hypertrophy.

To define the extent of left ventricular ejection and filling abnormalities in patients with mild hypertension, a non-imaging nuclear probe was used to generate high resolution time-activity curves in 25 patients with an average systolic blood pressure of 154 +/- 20 mm Hg and diastolic pressure of 98 +/- 8 mm Hg. The hypertensive patients did not meet electrocardiographic criteria for left ventricular hypertrophy, and none had evidence of ischemic or other cardiac disease. Compared with 25 age-matched normal subjects who had average systolic and diastolic pressures of 123 +/- 10 and 79 +/- 8 mm Hg, respectively, the hypertensive patients had a significantly lower ejection rate (2.00 +/- 0.20 versus 2.34 +/- 0.36 end-diastolic counts/s for the control group, p less than 0.05) and ejection fraction (58 +/- 4.9 versus 62 +/- 4.4) (p less than 0.05). The hypertensive patients had a markedly lower average rapid left ventricular filling rate (1.87 +/- 0.32 versus 2.69 +/- 0.41 counts/s for the control group, p less than 0.001). Although there was a modest inverse relation between echocardiographic left ventricular mass index and filling rate in the hypertensive patients (r = -0.59, p less than 0.01), 4 of 12 hypertensive patients with normal left ventricular mass index had a depressed filling rate. All of the hypertensive patients with increased left ventricular mass index had an abnormal left ventricular filling rate (less than 1.89 end-diastolic counts/s).(ABSTRACT TRUNCATED AT 250 WORDS)

Distal coronary artery injury following successful percutaneous transluminal coronary angioplasty.

A 65-year-old woman underwent successful percutaneous transluminal coronary angioplasty of a right coronary artery stenosis. Shortly thereafter, she developed chest discomfort and repeat angiography demonstrated a new area of stenosis distal to the area of original angioplasty. An attempt at a second angioplasty resulted in vessel occlusion with subsequent successful bypass surgery. The etiology of the new distal lesion is discussed.

Myocardial high-energy phosphate replenishment during ischemic arrest: aerobic versus anaerobic metabolism.

An in vivo, isolated pig heart preparation was used to study the effect of L-glutamate added to crystalloid and blood potassium cardioplegia on the myocardial high-energy phosphate compounds, adenosine triphosphate (ATP) and creatine phosphate (CP). Studies were performed during a three-hour arrest interval and during 60 minutes of reperfusion. Levels of ATP remained at or above control levels during arrest in animals receiving either unmodified blood or glutamate-enriched crystalloid cardioplegia. While glutamate significantly improved the ability of the crystalloid solution to preserve ATP during arrest, when added to blood, it contributed to a depressed ATP after a three-hour arrest. Creatine phosphate declined during arrest in all animals, but those receiving unenriched blood cardioplegia consistently had the highest levels (p less than 0.05). Addition of glutamate to crystalloid cardioplegia provided a significantly (p less than 0.05) higher level of CP at the end of three hours of arrest, which was still lower than that noted with unenriched blood. Comparable to its effect on the ATP level, when glutamate was added to blood cardioplegia, a decrease (p less than 0.05) in CP was noted after three hours of arrest. Attempts to enhance high-energy phosphate production by supplementing blood cardioplegia with L-glutamate are ineffective, while increased high-energy phosphate production results when glutamate is added to crystalloid cardioplegia. This implies that L-glutamate functions where anaerobic and not aerobic metabolism is the major component of preservation. With reperfusion, the only group of animals displaying depressed levels of ATP and CP was that receiving glutamate-enriched blood cardioplegia.

The effect of acute coronary artery occlusion during cardioplegic arrest and reperfusion on myocardial preservation.

A study was undertaken to evaluate the effect of acute occlusion of a coronary artery during cardioplegic arrest on myocardial preservation and to elucidate the influence of reestablishment of flow versus continued occlusion during the phase of myocardial reperfusion. Coronary occlusion was simulated, and myocardial viability was determined by measuring tissue levels of adenosine triphosphate (ATP) and creatine phosphate (CP) in biopsies of the posterior left ventricular wall. Eighteen pigs were divided into three equal groups consisting of animals with (1) patent right coronary arteries during arrest and reperfusion, (2) occluded right coronary arteries during arrest and patent during reperfusion, and (3) occluded right coronary arteries during arrest and reperfusion. The results of ATP and CP measurements showed that while poorer protection was afforded during two-hour arrest when the coronary artery was occluded, the risk of damage was much greater during reperfusion. Failure to restore adequate blood flow by retention of occlusion caused a concurrent decrease in ATP and CP levels below prescribed limits of myocardial tolerance. When occlusion occurs in the clinical setting, impeding cardioplegia and reperfusion, the importance of revascularization is emphasized.

The temperature dependence of recovery of metabolic function following hypothermic potassium cardioplegic arrest.

A study was performed to define the influence of reperfusate temperature on the recovery of high-energy phosphate compounds following hypothermic ischemic cardioplegic arrest. Two groups, each consisting of six pigs, were subjected to 1 hour of hypothermic potassium cardioplegic arrest (myocardial temperature 10 degrees to 15 degrees C). In one group, the arrest period was followed by a 30 minute period of normothermic reperfusion (37 degrees C) followed by a second hour of hypothermic cardioplegic arrest and a second 30 minute normothermic reperfusion period. The second group of pigs was reperfused after the first hour of arrest for 30 minutes with a cold blood (10 degrees to 14 degrees C) followed by an additional hour of hypothermic cardioplegic arrest and a second 30 minute hypothermic reperfusion period. Myocardial biopsy specimens for adenosine triphosphate (ATP) and creatine phosphate (CP) were obtained at the beginning of perfusion (control studies), at the end of each hour of the arrest interval, and at the end of each 30 minutes of reperfusion. The ATP and CP levels were significantly higher after normothermic reperfusion than after hypothermic reperfusion. After normothermic reperfusion the CP level exceeded control; following hypothermic reperfusion CP remained less than 70% of the control level. On the basis of these results, it is proposed that hypothermic reperfusion does not permit the same level of high-energy phosphorylation that is provided with normothermic reperfusion and may therefore adversely affect hemodynamic recovery of the heart after cardioplegic arrest.

Systolic time intervals in measurement of inotropic response to drugs.

During periods of tachycardia induced by atrial pacing in eight patients, moderate increments in dP/dt(max) and (dP/dt)/CPIP (common produced intraventricular pressure) and moderate reductions in left ventricular ejection time (LVET) and Q-S2 were demonstrated. These changes varied between individuals, but reduction in systolic intervals was consistently less than that reported from populations showing a range of resting heart rates. Individual regression formulae relating each variable to paced heart rate were used to calculate rate-dependent and rate-independent changes induced by isoprenaline and ouabain. Despite technical difficulty in precise measurement of systolic intervals, there was an excellent inverse correlation between rate-independent changes in Q-S2 and in both dP/dt(mac) and (dP/dt)/CPIP. Rate-independent change in Q-S2 appears to be a practical, moderately sensitive, and reasonably precise measure of the inotropic effect of a drug which does not radically alter left ventricular end-diastolic pressure or blood pressure. Day-to-day variation in systolic intervals may limit the use of the technique to studies of short duration.

Epicardial activation in human left anterior fascicular block.

Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal QRS axis more negative than -45 degrees, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior "fascicle" of the left bundle branch.

Left main coronary artery disease.

Eighteen patients with significant stenosis of the left main coronary artery are reported and compared with 1,040 patients described in the ten largest published series. In comparison to previous reports, our patients have a higher incidence of congestive heart failure, previous myocardial infarction (especially inferior wall), poorer left ventricular function, and more advanced coronary artery disease. Despite this, there was no increased risk during catheterization and bypass surgery. This small group of patients reflects the modern experience that, with increasing awareness of this lesion, there need not necessarily be a higher risk during diagnostic studies and therapeutic intervention.

Epicardial activation of the intact human heart without conduction defect.

To describe the epicardial ventricular activation sequence in the intact human heart, we obtained epicardial maps from 11 patients with normal QRS undergoing open heart surgery. Epicardial breakthrough (EBT), defined as the emergence of a radially propagating epicardial wavefront, occurred in three to five sites in each patient, and was earliest in the anterior right ventricle, 7--25 msec (mean 17 msec) after the onset of the QRS in all patients. Subsequent EBT occurred in the inferior right ventricle (10 sites in 10 patients), in the anterolateral left ventricle (13 sites in 10 patients), and the inferior left ventricle (eight sites in seven patients). Latest epicardial activation (LEA), defined as the latest site of recordable epicardial activity, occurred in the basal segments in all patients, anteriorly in the right ventricle in five patients, and inferiorly in six patients, four on the right and two on the left. LEA occurred 63--96 msec (mean 77 msec) after the onset of the QRS, and was recorded within 20 msec of the end of the QRS in all patients. Sequence of epicardial activation reflected a fusion process among the wavefronts. This descriptive and quantitative data should provide a suitable basis for comparison of abnormal ventricular activation sequences in patients undergoing surgery for preexcitation or ventricular tachycardia.

Recent insights into paroxysmal supraventricular tachycardia--an integrated approach to diagnosis and therapy.

Paroxysmal supraventricular tachycardia may result from re-entrance in the AV node, the normal A-V pathway with an accessory AV connection, in the sino-atrial node, in the atria, or else reflect ectopic impulse formation in a spontaneously automatic supraventricular focus. Electrocardiographic criteria which are helpful in differentiating these mechanisms involve an analysis of cycle length, changes in cycle length with intermittent bundle branch block, P wave morphology and the relationship of P wave to QRS complex, P-R interval, the presence of A-V block during tachycardia and the influence of autonomic tone on the tachycardia. Electrophysiologic studies further elucidate mechanism by demonstrating the mode of induction and termination of the tachycardia, the characteristics of antegrade and retrograde A-V conduction curves and refractory periods, atrial activation sequence of echo beats and the influence of premature beats introduced during tachycardia. These features are summarised in Table 1. Therapy can be accurately planned according to the results of experimental administration of antiarrhythmic agents and of pacing sequences upon induction and termination of tachycardia in the catheterisation laboratory.

Constrictive pericarditis due to methysergide therapy.

A 39-year-old woman who suffered from migraine is described. She developed analgesic nephropathy due to phenacetin, and constrictive pericarditis, probably due to methysergide treatment.