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PubMed1986

Chemical ablation of ventricular tachycardia in the dog.

Sustained ventricular tachycardia was induced in dogs following occlusion-reperfusion of the left anterior descending coronary artery. While dogs were supported by cardiopulmonary bypass, the left ventricle was opened and the endocardium was mapped during electrically induced ventricular tachycardia to determine the earliest site of ventricular activation. Phenol (carbolic acid) application at that site necrosed myocardium to a depth of 1 to 3 mm and prevented electrical reinduction of ventricular tachycardia in 9 of 15 dogs. These data suggest that chemical ablation may be used as an alternate means to destroy areas of myocardium involved in the genesis or maintenance of ventricular tachycardia, particularly if these areas cannot be resected surgically because of their size or location.

Animals↗
PubMed1987

Left ventricular systolic circular index: an echocardiographic measure of transseptal pressure ratio.

An echocardiographic index of left ventricular (LV) short axis circularity can be defined by the equation: left ventricular systolic circularity index (LVSCI) = 4 pi(LV area) X 100/(LV perimeter). This index was measured from two-dimensional echocardiograms in 98 children (ages 1 day to 19 years) with congenital heart disease, and results were compared to right ventricular/left ventricular peak systolic pressure ratios (RVP/LVP) determined at cardiac catheterization. LVSCI was also computed in 50 children without cardiovascular or pulmonary disease to define the normal range. A short axis image of the left ventricle at the level of the papillary muscles was obtained from the left parasternal position. Area and perimeter were determined by computer planimetry of the LV endocardium at end systole. LVSCI was measured from three consecutive beats and averaged. In the normal group all values of LVSCI exceeded 93% (mean 96%). In the group with congenital heart disease RVP/LVP correlated exponentially with LVSCI: RVP/LVP = e2.6-0.04 LVSCI; with r = 0.88, SEE = 0.39, and p less than 0.001. If patients with suprasystemic right ventricular pressures (RVP/LVP greater than 1.2) are excluded, there is a linear correlation between RVP/LVP and LVSCI: RVP/LVP = 2.3-0.021 LVSCI; with r = 0.80, SEE = 0.14, and p less than 0.001. LVSCI could distinguish between patients with normal, mildly elevated, moderately elevated, and severely elevated RVP/LVP. We conclude that LVSCI is a readily determined parameter that is independent of age or body size and predicts RVP/LVP in children with congenital heart disease.

Adolescent↗
PubMed1994

Infantile histiocytoid cardiomyopathy: three cases and literature review.

A review is presented of the clinical and cardiac morphologic findings in 50 previously reported and 3 new patients with histiocytoid cardiomyopathy. This disorder occurs in infants and small children and is characterized clinically by severe and often fatal arrhythmias and morphologically by focal collections of altered myocytes that are roundshaped and resemble histiocytes. Sixteen patients had yellowish nodules on the endocardium, epicardium, and/or valves; the other 37 had foci of abnormal myocytes throughout the myocardium. These cells were remarkably similar in all patients and had poorly developed or absent intercellular junctions, few or no contractile elements, and markedly increased numbers of mitochondria, which imparted a granular or vacuolated appearance to the cytoplasm. There was a high prevalence of anomalies involving the nervous system and eyes and of oncocytic cells in various glands. Evidence is presented to exclude the possibilities that the disorder represents a developmental anomaly of the atrioventricular conduction system, a multifocal tumor of Purkinje cells, a developmental arrest of cardiac myocytes, and a diffuse type of mitochondrial cardiomyopathy. Histiocytoid cardiomyopathy is considered to be the result of hamartoma-like aggregations of cardiac myocytes with features similar to those of oncocytes. This syndrome is likely caused by prenatal myocardial or systemic (viral?) injury. Surgical excision of nodules of histiocytoid cells can result in clinical remission.

Cardiomyopathies↗
PubMed1994

Reperfusion enhances the local release of endothelin after regional myocardial ischemia.

The role of endothelin, a potent long-acting vasoconstrictor peptide, in the pathogenesis of the "no-reflow" phenomenon was investigated in nine closed-chest mongrel dogs undergoing 90 minutes of proximal left anterior descending artery occlusion and 3.5 hours of reperfusion. Endothelin levels were measured serially from the coronary sinus (CS) and aorta (Ao) by radioimmunoassay and correlated with regional myocardial blood perfusion. Prolonged anesthesia, surgery, and vascular instrumentation did not change endothelin levels in four sham animals. A progressive and parallel increase in CS and Ao endothelin levels occurred during coronary occlusion. A further increase in CS levels was observed during the reperfusion period, resulting in significantly higher values of the peptide at 30 and 60 minutes (30 minutes: CS 22.1 +/- 3.5 vs Ao 15.1 +/- 5.1 pg/ml; 60 minutes: CS 21.1 +/- 4.5 vs Ao 15.0 +/- 3.6 pg/ml; p < 0.05 by analysis of variance). Microvascular perfusion determined semiquantitatively with fluorescent beads was significantly reduced in the central ischemic zone (CIZ) compared with that in the nonischemic zone (NIZ) (CIZ endocardium 1.14 +/- 0.4 beads/m2, CIZ midmyocardium 1.19 +/- 0.3 beads/m2, NIZ 3.8 +/- 0.6 beads/m2; p < 0.05). A significant correlation was noted between mean reperfusion levels of endothelin in the CS and endocardial flow in the CIZ (r = -0.88; p = 0.009). This study demonstrates that reperfusion per se enhanced the spillover of endothelin from the cardiac interstitium. Local release of endothelin may contribute to the progressive decrease in microvascular flow in the reperfused bed.

Animals↗
PubMed1975

Cardiac pathology after valve replacement by disc prosthesis. A study of 61 necropsy patients.

Clinical and necropsy observations are described in 61 patients who had one or more cardiac valves replaced with a discoid prosthesis of the Hufnagel type. The most common (31 percent) cause of death among the 45 patients who died early (less than 65 days after operation) appeared to be prosthetic disproportion; that is, the prothesis was too big for the aorta or ventricular cavity into which it was inserted so that inadequate space was present between the margins of the disc and the endocardium of ventricle or intima of aorta. Prosthetic thrombosis occurred in only 3 of the 45 patients who died early, but poppet movement appeared considerably altered in each. In contrast, thrombi were observed on a prosthesis in 14 of the 16 patients who died late (4 to 47 months [average 21] postoperatively), but in none did the thrombi appear of sufficient size to alter poppet function. Escessive bleeding occurred in 11 (24 percent) of the 45 early deaths and was primarily related to the insertion of a patch in the root of the aorta. Uncorrected valvular disease either by itself or by its ability to alter function of the prosthesis appeared responsible for death in 6 (13 percent) of the 45 patients who died early and in 2 (6 percent) of the 16 who died late. Insertion of a mitral poppet disc in a patient with uncorrected aortic regurgitation, even of mild degree, may be hazardous because the aortic regurgitant jet stream may interfere with proper function of the mitral disc. Likewise, insertion of a poppet disc only in the aortic valve position in a patient with combined aortic and mitral regurgitation may considerably increase the degree of mitral incompetence because the aortic prosthesis is intrinsically obstructive. Disc wear or variance was observed in all but one prosthesis in place for more than 1 year. Although hemolytic anemia of significant degree was not observed in any of the 16 patients who died late, the occurrence of renal hemosiderosis in 13 of the 16 patients indicates that the poppet disc prosthesis is considerably traumatic to erythrocytes. Thus, this type of prosthesis is not an ideal substitute cardiac valve. It clots, despite anticoagulant therapy, it is intrinsically stenotic, portions of it, that is, the disc, degenerate, and it causes hemolysis to erythrocytes.

Adult↗
PubMed1976

Effect of vagus nerve stimulation upon excitability of the canine ventricle. Role of sympathetic-parasympathetic interactions.

The effect of vagus nerve stimulation on ventricular excitability was studied in 28 dogs under various conditions of adrenergic neural tone. Strength-interval curves were delineated from the apex of the right ventricular endocardium with a transvenous bipolar catheter. Vagus nerve stimulation in both closed chest and open chest dogs shifted the strength-interval curve 6 to 8 msec later into electrical diastole (P less than 0.001). Left stellate ganglion stimulation shifted the strength-interval curve 9 to 11 msec earlier into diastole (P less than 0.001). The effect of simultaneous left stellate ganglion and vagus nerve stimulation was not significantly different from that of left stellate ganglion stimulation alone. The influence of vagus nerve stimulation on the strength-interval curve under basal conditions was abolished by acute beta adrenergic blockade with propranolol. It is concluded that vagus nerve stimulation affects ventricular excitability as well as vulnerability by opposing the effects of sympathetic neural tone.

Adrenergic beta-Antagonists↗
PubMed1978

Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion.

The progressive transmural electrographic, biochemical and ultrastructural changes as a function of time after acute coronary occlusion were systematically assessed in eight dogs. Transmural plunge electrodes with poles 1 mm apart were placed in the ischemic and nonischemic zones, and coronary occlusion was maintained for 4 hours. Transmural full thickness biopsy specimens were obtained from each zone for electron microscopy before, and 1 and 4 hours after occlusion. Endocardial and epicardial layers were also obtained for assessment of myocardial potassium ion (K+) and sodium ion (Na+) concentrations. Before coronary occlusion, local Q waves were recorded an average depth of 1.0 +/- 0.34 mm from the endocardial surface. After 1 hour of occlusion, Q waves appeared at an average depth of 3.8 +/- 0.67 mm and progressed to a depth of 5.2 +/- 0.7 mm at 2 hours, 6.2 +/- 0.5 mm at 3 hours and 7.0 +/- 0.5 mm at 4 hours. After 1 hour, ultrastructural changes of early ischemia, including a decrease in glycogen and mild mitochondrial swelling, were seen in the endocardial layer; the epicardial layer showed normal morphologic features. After 4 hours, the endocardial layer showed well developed ischemic changes marked by the loss of mitochondrial cristae, vacuolization, the appearance of amorhopous mitochondrial cristae, vacuolization, the appearance of amorphous mitochondrial densities, an increase in interfibrillary space and the appearance of I bands. In contrast, the epicardial layer at this time showed only early ischemic changes. At the end of 4 hours, the endocardial layer showed a marked decrease in myocardial K+ concentration and an increase in Na+ concentration leading to complete reversal of K+/Na+ ratio (0.7 +/- 1.0; P less than 0.001). In the epicardial layer, a smaller decrease in K+ concentration and an increase in Na+ concentration occurred, resulting in a diminution but not a reversal of K+/Na+ ratio (1.4 +/- 0.2; P less than 0.005). Thus, the dynamic evolution of an acute myocardal infarction involves a sequential progression from endocardium to epicardium as a function of time, resulting in an epicardial "border zone" in the early stages after acute coronary occlusion.

Animals↗
PubMed1979

Mural vegetations at the site of endocardial trauma in infective endocarditis complicating idiopathic hypertrophic subaortic stenosis.

In two patients infective endocarditis developed as the primary manifestation of idiopathic hypertrophic subaortic stenosis. Infected vegetations were present on the mitral and aortic valves. In addition, bacterial vegetations were observed on the septal endocardium at the site of contact between the mitral valve leaflet and the hypertrophic septum. Thus, chronic endocardial trauma, a common finding in idiopathic hypertrophic subaortic stenosis, may provide a fertile nidus for the development of bacterial vegetation.

Aged↗
PubMed1981

Observations on detecting left ventricular thrombus with two dimensional echocardiography: emphasis on avoidance of false positive diagnoses.

Observations made in detecting left ventricular thrombus with two dimensional echocardiography in 25 patients are reviewed. In 20 patients thrombus was documented on angiography, surgery postmortem examination or serial two dimensional echocardiographic findings; in the remaining five patients two dimensional echocardiographic findings of thrombus were unequivocal. In all 25 patients wall motion abnormalities ranging from hypokinesia to frank dyskinesia were present at the site of the thrombus. Twenty-three patients had an apical thrombus; two had thrombus adjacent to the inferior wall. Clear delineation of the endocardium and thrombus margin was considered essential to the correct diagnosis of thrombus. Both intracavitary motion of the thrombus margin and a layering effect were noted infrequently although they were of benefit in identifying an intracardiac mass as thrombus. In addition, serial evaluations were helpful in establishing the correct diagnosis. False positive diagnoses can be minimized if one understands certain technical limitations of this method and correctly identifies apical structures that are not thrombi. Axial and lateral resolution problems inherent with this technique can produce intracavitary echoes that may simulate thrombi. In addition, normal or pathologic structures at the apex may also simulate thrombi. These structures include the papillary muscles, muscular trabeculae, chordal structures and tangential information from normal myocardium. Varying the sector orientation or acoustic window, or both, will aid in correctly identifying these structures and distinguishing them from left ventricular thrombi.

Blood Coagulation↗
PubMed1981

Effects of diltiazem on conduction of premature impulses during acute myocardial ischemia and reperfusion.

The effect of diltiazem on conduction of cardiac impulses was studied using premature impulses. Conduction times were measured in the epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion of the left ventricular anterior wall. In 16 dogs (8 control and 8 treated with diltiazem), the left anterior descending artery was occluded initially below the second diagonal branch and 30 minutes later below the first diagonal branch. Infusion of diltiazem (0.02 mg/kg per min) was begun at the time of the first ligation in the treated dogs. Conduction delay in normal, ischemic and reperfused myocardium and at the border of ischemia or reperfusion was compared in the two groups. In addition, treated and nontreated ischemic zones were analyzed in the diltiazem-treated group. Results show significantly less ischemia-induced conduction delay in the diltiazem-treated group in both ischemic myocardium and at the border of ischemia. This beneficial effect was seen in the ischemic segment in the treated dogs whether or not the medication was given before or after coronary ligation. Further, the effect of the drug on epicardial and endocardial conduction did not differ significantly. These data suggest that diltiazem may have potential value in the treatment of ventricular reentrant arrhythmias associated with acute ischemia over and above the well recognized hemodynamic and metabolic effects of calcium channel blocking agents.

Animals↗
PubMed1982

Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia.

Intraoperative pace-mapping has been proposed as a method of identifying the origin of ventricular tachycardia; however, both epicardial activation and electrocardiographic configuration have limitations in localizing the origin of ventricular tachycardia. Because most ventricular tachycardias associated with ischemic heart disease appear to arise near the endocardium, this study evaluated the ability of bipolar catheter endocardial pacing at or near the endocardial site of origin of spontaneous ventricular tachycardia to mimic the QRS configuration of the spontaneous tachycardia. Twelve patients were studied who had ventricular tachycardia whose origin was determined with catheter endocardial mapping. Three patients had ventricular tachycardia with two distinct configurations. The electrocardiogram of ventricular tachycardia was compared with the electrocardiogram produced by pacing at the site of origin (10 patients) and at multiple (two to nine) additional sites in 8 patients. It was observed that (1) pacing at the known site of origin of ventricular tachycardia produced an electrocardiogram and activation sequence similar to those produced by the ventricular tachycardia; (2) pacing at sites in close proximity to the site of origin of ventricular tachycardia produced either a similar or a grossly different electrocardiographic pattern from that during ventricular tachycardia. It is concluded that catheter endocardial pace-mapping (1) is a corroborative method of identifying the origin of ventricular tachycardia; (2) may be useful in patients with noninducible ventricular tachycardia or rapid ventricular tachycardia who cannot undergo catheter or intraoperative mapping; and (3) is neither easier, more accurate nor quicker than direct localization by mapping during ventricular tachycardia.

Adult↗
PubMed1982

Role of catheter mapping in the preoperative evaluation of ventricular tachycardia.

Although surgery is an accepted mode of therapy for refractory ventricular tachycardia, routine aneurysmectomy has yielded unpredictable results. This is believed to have occurred because there was no documentation that the arrhythmia actually arose from resected aneurysmal tissue. Catheter endocardial mapping has been used to localize preoperatively the area of origin of the arrhythmia. This technique has established that the arrhythmias arise near the endocardium at the borders of the aneurysm or infarction, or both. These regions, particularly when they occur in the interventricular septum, are not resected by standard aneurysmectomy. Intraoperative endocardial and epicardial mapping have validated the accuracy of this technique. We believe that catheter mapping should be performed before surgery for the following reasons: (1) In some patients ventricular tachycardia is not inducible in the operating room (for example, automatic ventricular tachycardia can be mapped in the catheterization laboratory); (2) in some patients not all morphologic forms of tachycardia can be induced or mapped intraoperatively because of failure of inducibility, time constraints or degeneration of the arrhythmia to ventricular fibrillation; and (3) intraoperative endocardial mapping occasionally cannot be performed because of lack of technical skills, physical factors such as mural thrombosis, or the inability to induce ventricular tachycardia after aneurysmectomy. Other methods currently being evaluated to localize the origin of ventricular tachycardia that do not require induction of arrhythmia are analysis of ventricular electrograms during sinus rhythm and pacemapping.

Cardiac Catheterization↗
PubMed1982

Effects of amyl nitrite on left ventricular relaxation in patients with borderline hypertension.

The effects of systemic hypertension on left ventricular relaxation properties remain largely undefined. To assess such effects 22 normal volunteers and 15 patients with borderline hypertension were examined. The tangent to the echocardiographic left ventricular posterior wall endocardium was measured in diastole and was normalized for end-diastolic dimension to yield normalized velocity of relaxation. This velocity of relaxation was measured at rest and throughout inhalation of amyl nitrite. Mean value +/- standard deviation (SD) from rest to peak amyl nitrite effect for the normal group and for the patients with borderline hypertension was 3.3 +/- 0.6 leads to 7.2 +/- 1.1 and 3.0 +/- 0.8 leads to 4.4 +/- 1.1 s-1, respectively. All 22 persons in the normal group and 2 of the 15 patients with borderline hypertension attained normalized velocity of relaxation greater than 5.5 s-1 with administration of amyl nitrite. Multivariate analysis in the normal group identified heart rate, mean arterial pressure, and fractional shortening as the best predictors of normalized left ventricular relaxation velocity (r = 0.85; p less than 0.001). The increase in the normalized velocity of relaxation induced by amyl nitrite is blunted in patients with borderline hypertension. These changes in left ventricular relaxation identify early cardiac involvement and may prove clinically useful in hypertensive patients.

Adult↗
PubMed1982

Epicardial activation of the human ventricle: effects of left ventricular hypertrophy.

To determine the effects of left ventricular hypertrophy on epicardial activation of the human heart, intraoperative epicardial mapping of 40 to 66 points was performed in 10 patients undergoing aortic valve replacement. Mean calculated left ventricular mass was 364 +/- 98 g. All patients had normal left ventricular contraction. Earliest epicardial activation occurred in the anterior right ventricle in all patients. In 9 patients, it was the only epicardial breakthrough point. One patient had a single inferior left ventricular breakthrough point. Epicardial activation spread from the right ventricle towards the left ventricle in both the anterior and inferior direction. Latest epicardial activation occurred at the base of the left ventricle in 9 patients and the base of the right ventricle in 1. When compared with patients with coronary artery disease, normal ventricular contraction, and no left ventricular hypertrophy, patients with hypertrophy had fewer left ventricular breakthrough points (p less than 0.001) and were more likely to have latest activation at the left ventricular base (p less than 0.0010. We conclude that left ventricular hypertrophy is associated with marked changes in the pattern of epicardial activation. These changes may reflect delay in spread from endocardium due to the increased wall thickness.

Adult↗
PubMed1983

Sympathetic denervation limited to a region of acutely ischemic canine myocardium increases excitability threshold and duration of bipolar electrograms.

This study determines the direct effects of sympathetic denervation on excitability threshold and bipolar electrograms in acutely ischemic myocardium. Regional denervation was performed by application of phenol to the epicardium surrounding the ischemic zone in order to eliminate the possible hemodynamic effects that global cardiac denervation may exert on the ischemic zone. Data were obtained during serial occlusions (less than or equal to 6 minutes in duration) of left anterior coronary artery in open-chest dogs with sympathetic denervation performed before the last occlusion. Late diastolic threshold was measured every 5 seconds by a constant voltage pacemaker which automatically registered threshold in stimulus duration. During ischemia, regional denervation (n = 9) increased peak excitability threshold from 240 +/- 51 (standard error of the mean) to 552 +/- 182 mus (p less than 0.05) and prolonged electrographic duration in epicardium from 19 +/- 3 to 25 +/- 4 ms (p less than 0.025) and in endocardium from 20 +/- 3 to 25 +/- 4 ms (p less than 0.01). Phenol application did not alter aortic pressure, ischemic wall motion (sonomicrometer technique), or ischemic zone blood flow (microsphere technique). Thus, acute sympathetic denervation when limited to ischemic myocardium increases the peak excitability threshold and concomitantly prolongs duration of bipolar electrograms.

Animals↗
PubMed1983

Diastolic synchronized retroperfusion versus reperfusion: effects on regional left ventricular function and myocardial blood flow during acute coronary occlusion in dogs.

The effects of 170 minutes of diastolic synchronized retroperfusion of the coronary sinus with arterial blood during 180 minutes of coronary artery occlusion on regional myocardial contractility (ultrasonic crystals) and blood flow (microspheres) were investigated in open-chest dogs. These effects were compared with those of 180 minutes of coronary occlusion and those of 170 minutes of anterograde reperfusion after 10 minutes of coronary occlusion in separate groups of dogs. Retroperfusion was able to almost restore transmural blood flow in the moderately ischemic zones and to increase it back to 47% of its preocclusion value in the severely ischemic zones with, in both zones, a favorable redistribution of flow toward the endocardium. Simultaneously, retroperfusion significantly improved segment length shortening in the moderately ischemic zones and significantly reduced the extent of paradoxical bulging in the severely ischemic zones. These partial recoveries in regional contractility and blood flow during retroperfusion were intermediate between those induced by 170 minutes of anterograde reperfusion and those of 180 minutes of coronary artery occlusion. Thus, in the presence of coronary artery occlusion, retroperfusion appears to exert a beneficial effect by improving both regional perfusion and function in the ischemic zones and may be proposed as a medical circulatory support to the jeopardized myocardium.

Acute Disease↗
PubMed1984

Computer-assisted edge detection in two-dimensional echocardiography: comparison with anatomic data.

Four methods of computer-based edge detection were evaluated for identification of endocardial and epicardial borders on 2-dimensional echocardiograms of excised hearts. A method was also evaluated for observer identification of cardiac borders in the same hearts. The accuracy of computer-derived borders and of observer-derived borders were determined by comparison to anatomic borders measured from photographs of slices of the excised hearts. Echocardiographic borders were compared with anatomic borders by calculation of segmental cavity areas and wall thickness. Each of the methods tested (computer and observer) identified endocardial borders accurately, resulting in cavity segment areas that correlated well with the corresponding anatomic data (r = 0.90 to 0.92). Regional wall thicknesses correlated less well with anatomic data (r = 0.74 to 0.80), suggesting that endocardial borders were identified more accurately than were epicardial borders. Thus, the methods of computer-assisted echocardiographic border detection tested identified the endocardium and epicardium as accurately as a trained observer evaluating unprocessed echocardiograms. Computer-based methods of border detection may be useful in the automated analysis of clinical echocardiograms.

Animals↗
PubMed1984

Correlates of reperfusion ventricular fibrillation in dogs.

To elucidate determinants of reperfusion ventricular fibrillation (VF), regional myocardial blood flow, ATP, creatine phosphate (CP), heart rate and blood pressure were compared in 2 groups of anesthetized dogs: those that fibrillated spontaneously upon release of a 15-minute coronary artery occlusion (VF group, n = 8) and those that did not fibrillate when reperfused (No VF group, n = 27). Arterial pressure and heart rate before and during coronary artery occlusion were similar in both groups. Ischemic endo- and epicardial ATP values, measured at the end of the occlusion period, were reduced approximately 20% of nonischemic values in both groups. In contrast, CP (nmol . mg protein-1) within the ischemic zone was significantly lower in the VF group in both the epicardium (14.3 +/- 1.6 in the VF group vs 22.8 +/- 2.5 in the No VF group, p less than 0.01) and the endocardium (9.0 +/- 2.0 in the VF group vs 18.7 +/- 1.8 in the No VF group, p less than 0.01). Furthermore, epi- and endocardial regional myocardial blood flow in the center of the ischemic zone during occlusion was significantly lower in VF dogs than in No VF dogs. Epicardial flow was 0.06 +/- 0.03 ml X min-1 X g-1 in VF dogs vs 0.44 +/- 0.06 in No VF dogs (p less than 0.001) and endocardial flow was 0.03 +/- 0.02 ml X min-1 X g-1 in VF dogs vs 0.23 +/- 0.04 ml X min-1 X g-1 in No VF dogs (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗