- Email: [email protected]
Polymorphous ventricular tachycardia early after acute myocardial infarction
disc manifestations in common. A 43-year-old woman, with a history of malignant GCT with documented metastases to bones and lymph nodes presented with severe bradycardia. Electrocardiography showed complete heart block with a normal atria1 rate, alternating with a right bundle branch block pattern with left anterior fascicular block, requiring a permanent pacemaker placement. Myocardial biopsy showed severe inliltration of myocardial tissue by GCT. Although rare, both benign and malignant GCTs can cause symptomatic cardiac involvements, all of which have been those of conduction system dysfunction. Kenichi
Fujise,
MD
New York, New York 12 March 1993 1. Wang J, Kragel AH, Friedlander ER, Cheng JT. Granular cell tmnor of the sinus node. Am .I Cardiol 1993;71:49@491. 2. Roth D, Spain DM. Granular-cell myoblastoma of the mycca~dium: case report. Cancer 19X&5:302-306. 3. Fenoglio JJ Jr, McAllister HA Jr. Granular cell tumors of the heaxt. Arch Path01 Lab Med 1976; 100:
a critical care update conference. As I am a pulmonologist by training, I ventured into the cardiology literature to prepare myself. The following poem summarizes my reaction to the overwhelming number of thrombolytic trials. I suspect one would need to write an epic to include all the acronyms listed by Cheng.’ Recital note: ECGS should be spelled out while the other acronyms should be pronounced. Lytic Lament ECGS GUSTO ISIS are some of the trials of thrombolysis
ASSETEMERAS TPAT HART just a few more and I’m sure I’ll be smart TIMI TAMI MlTI GISSI I’ve read them all but alas I’m just dizzy James
R. Gossage,
MD
Nashville, Tennessee 19 April 1993 1. Cheng TO. Acronyms Am J Cardiol
of major cardiologic trials.
1992:70:1512-1513.
U&278. 4. O’Conell
DJ, MacMahon H, De Mess& TR. Multicentric tracheobronchial and oesophageal granular cell myoblastoma. Thorax 1978;33:596-602. 5. Khanolkar VR Granular cell myoblastoma. Am .I
Relation Between Patent Foramen Ovale and Stroke
Path01 1947;23:721-739.
Svejda J, Horn V. Disseminated granular-cell pseudotumor: so-called metastasizing granular-cell myoblastoma. .I Path01 1958;76:343-348. 7. Kubac G, Doris I, Ondro M, Davey PW. Malignant granular cell myoblaatoma with metastatic cardiac involvement; case report and echocardiogram. Am Heart J 1980; 100~227-229. 6. Ravich A, Stout AP, Ravich RA. Malignant granular cell myoblastoma involving the urinary bladder. Ann Surg 1945;121:361-372. 6. Kreig AF. Malignant granular cell myoblastoma. 6.
Arch Pathol 1962;74:252-256. 10. Mackenzie DH. Malignant granular cell myoblastoma. J Clin Pathol 1967;20:739-742.
il. Usui M, Ishii S, Yamawaki S, Sasaki T, Minami A, Hizawa K. Malignant granular cell hunor of the radial nerve. An autopsy observation with electron microscopic and tissue culture studies. Cancer 1977; 39:1547-1555.
12. Steffelaar JW, Nap M, Ha&t UJGM. Malignant granular cell tumor. Am J Sur-g Path01 1982;6:665-672.
Lytic Lament
A recent letter to The American Journal of Cardiology provided a prodigious list of acronyms for major clinical trials in cardiology.1 Although incomplete, the list contained over 200 entries! It is unclear to me whether the authors meant to provide a service or humor, but I wish to stray to the lighter side. I was recently asked to give a talk on thrombolysis in acute coronary ischemia at
In their article on the relation between patent foramen ovale (PFO) and unexplained stroke, Van Camp et al’ conclude that early and massive passage of contrast in the left atrium through a PFO is a possible mechanism for stroke. However, 38% of the patients in the stroke group and 25% of the patients in the control group had atrial fibrillation which, by itself, is a major risk factor for stroke.2 They should have excluded patients with atria1 fibrillation in both groups before analyzing the data. If, after exclusion of the 18 patients with atrial fibrillation, the remaining patients show a signilicantly higher incidence of abnormal PFO morphology with early and massive passage of contrast, only then is their conclusion regarding the relation between PFO and stroke valid. Anil
K. Mukeriee.
West Roxbury
Polymorphous Ventricular Tachycardia Early After Acute Myocardial Infarction
The article by Bimbaum and colleagues’ describing polymorphous ventricular tachycardia early after acute myocardial infarction pointed out some important aspects of this condition. However, no mention was made about the role of magnesium in the etiology or treatment of the patients described in that report. Polymorphous ventricular tachycardia in this setting has been reported to respond to magnesium supplementation when other antiarrhythmic drugs failed to stabilize the cardiac rhythm.2 Polymorphous ventricular tachycardia in other clinical settings has also been shown to be associated with magnesium deficiency and respond to intravenous infusion of magnesium.3~4 Magnesium is predominantly an intracellular cation5 with little correlation being found between the measured serum concentration and the intracellular concentration.c8 A role magnesium plays in metabolism is that of a regulator of other ions; this action occurs within the cell at the molecular level and on the cell membrane.9 There is a particularly close relation between intracellular magnesium and potassium.1° The antiarrhythmic or membrane-stabilizing effect of magnesium may be related to its ability to regulate internal potassium homeostasis. l1 Because the serum magnesium concentration does not give an accurate assessment of the magnesium status of a patient, empiric use of magnesium supplementation should be considered in settings known to be associated with magnesium depletion.12 Magnesium is well tolerated when given intravenously, particularly when renal function is not impaired, is effective in a variety of settings, is readily available and is inexpensive. Richard
A. Reinhart,
Marsh6eld,
MD
Mass&h&etis 13 May 1993
MD
Wisconsin 18 May 1993
596598. 2. Petersen
1. Bimbaum Y, Sclarovsky S, Ben-Ami R, Rechavia E, Strasberg B, Kusniec J, Mager A, Sulkes J. Polymorphous ventricular tachycardia early after acute myocardial infarction. Am J Cardiol 1993;71:745-750. 2. Friday BA, Reinhart R4. Magnesium metabolism: a case report and literature review. Crit Care Nurse
1990;819.
3. Ramee SR, White CJ, Svinzuich JT, Watson TD,
1. Van Camp GV, Schulze D, Cosyns B, Vanden-
bossche J-L. Relation between patent foramen ovale and unexplained stroke. Am J Cardiol 1993;71: P. Risk factors for thromboembolic complications in chronic atria1 fibrillation. Arch Intern Med
1991;11:62-72.
READERS COMMENTS 863
Fox RF. Torsades de pointes and magnesium de& ciency. Am Heart J 1985;109:1@-166. 4. Tzivoni D, Keren A, Cohen AM. Magnesium therapy for tormdes de pointes. Am J Cardiol 1984,53: 528-530. 5. Reinlxut RA. Magnesium metabolism: a review with special reference to the relationship between intracellular content and senxn levels. Arch Intern Med 1988;148:2415-2420. 6. Reinhart RA, Marx Jr JJ, Haas RG, Desbiens NA. Inkw.llular magnesium of mononuclear cells from venous blood of clinically healthy subjects. Clin Chim Acta 1987;167:187-195. 7. Reinhart RA, Marx Jr JJ, Broste SK, Haas RG. Myocardial magnesium: relation to laboratory and clinical variables in patients undergoing cardiac surgery. J Am Coil Cardiol 1991;17:651-656, 8. Reinhart RA, Fananapazir L, Cannon Ill RO, Hosseini JM, Elin RJ. Effect of intravenous magnesium sulfate. on blood magnesium parameters. Mqnes Trace Elem 1990;9:191-197. 9. Reinhart RA. Clinical correlates of the molecular and cellular actions of magnesium on the caxliovascular system. Am Heart J 1991;121:1513-1521. 10. Reinhart RA, Broste SK, Spencer S, Marx Jr JJ, Haas RG, Rae P. Relation between magnesium and potassium concentrations in myocardium, skeletal muscle, and mononuclear blocd cells. Clin Chem 1992~38: 2444-2448. 11. white RE, Hartzell HC. Magnesium ion in cardiac function: regulator of ion channels and second messengers. Biochem Phmmacol 1989;38:859-867. 12. Reinbart RA. Magnesium deficiency: recognition and treatment in the emergency medicine setting. Am J Emerg Med 1992;10:78-83.
Prognostic Significance and the Role of DualChamber Pacing in Atrioventricular Delay in Idiopathic Dilated Cardiomyopathy
I read the report by Schoeller et al,’ which described lirst- or second-degree atrioventricular (AV) block as an independent risk factor in patients with idiopathic dilated
864
cardiomyopathy @DC). Their report has added rational data for the development of dual-chamber pacemaker therapy in patients with IDC, which was lirst used by Hochleitner et al2 and mysehT3 A subsequent report by Hochleitner et al4 described improved survival in IDC patients with dual-chamber pacing. It is expected that dual-chamber pacing would lead to a better clinical outcome in many IDC patients with AV delay. The exact mechanism(s) by which dual-chamber pacing improves the compromised hemodynamics in patients with IDC is still unclear, but my previous experience3 has shown that optimal AV setting using dual-chamber pacing can improve left ventricular function by producing an increase in left ventricular filling, thus promoting the use of the Frank-Starling mechanism in IDC patients with lirst-degree AV block. Elimination of the AV valve regurgitation by dual-chamber pacing with a short AV interval should also be considered.5 Unexpected cardisc events due to further progression of AV block would be preventable by the placement of a dualchamber pacemaker in IDC patients with first- or second-degree AV block. The beneficial effect of padrenergic-blocking therapy in IDC has been con6rmed,6 but the presence of AV delay would compromise this therapy. Implantation of a dual-chamber pacemaker would not
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 72
OCTOBER 1,1993
only improve cardiac function in itself, but also facilitate safe p-adrenergic-blocking therapy. Thus, it is expected that dual-chamber pacing would improve the prognosis of lDC patients with lirst- or second-degree AV b1ock.l Given the relatively frequent manifestation of lirst- or second-degree AV delay and its prognostic significance in IDC,’ systematic study should be done to determine the indications for dual-chamber pacing in patients with IDC. Hajime
Kataoka, MD Saiki-city, Japan 20 April
1993
1. Schoeller R, Andresen D, But&x P, Oezcelik K, Vey G, Scbroder. First- or second-degree &oventricular block as a risk factor in idiopathic dilated cardiomyopathy. Am J Cardiol 1993;71:720-726. 2. Hochleitner M, H&tnagl H, Ng CK, Hijrtnagl H, Gschnitzer F, Zechmann W. Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. Am J Cardiol 1990;66: 1cm--m? 3. Kataoka H. Hemodynamic effect of physiological dual chamber pacing in a patient with end-stage dilated cardiomyopathy: a case report. PACE 1991;14: A,”
a”*.
133~435.
4. Hochleitner M, Htirtnagl H, Hiilblagl H, Fridrich L, Gscbnitzer F. Long-term efficacy of physiologic dual-chamber pacing in the treatment of end-stage idiopathic dilated cardiomyopathy. Am J Cardiol1992; 70:132&1325. 5. Brecker SJD, Xiao HB, Sparrow J, Gibson DG. Effects of dual-chamber pacing with short ahioventricular delay in dilated cardiomyopathy. Lancet 1992;340:1308-1312. 6. Waagstein F, Caidahl K, Wall&in I, Be@ CH, Hjalmarson A. Long-term p-blockade in dilated cardiomyopathy: effects of short- and long-term metopro101 treatment followed by withdrawal and readministration of metoprolol. Circulation 1989;80: 551-563.
Fujise,
MD
New York, New York 12 March 1993 1. Wang J, Kragel AH, Friedlander ER, Cheng JT. Granular cell tmnor of the sinus node. Am .I Cardiol 1993;71:49@491. 2. Roth D, Spain DM. Granular-cell myoblastoma of the mycca~dium: case report. Cancer 19X&5:302-306. 3. Fenoglio JJ Jr, McAllister HA Jr. Granular cell tumors of the heaxt. Arch Path01 Lab Med 1976; 100:
a critical care update conference. As I am a pulmonologist by training, I ventured into the cardiology literature to prepare myself. The following poem summarizes my reaction to the overwhelming number of thrombolytic trials. I suspect one would need to write an epic to include all the acronyms listed by Cheng.’ Recital note: ECGS should be spelled out while the other acronyms should be pronounced. Lytic Lament ECGS GUSTO ISIS are some of the trials of thrombolysis
ASSETEMERAS TPAT HART just a few more and I’m sure I’ll be smart TIMI TAMI MlTI GISSI I’ve read them all but alas I’m just dizzy James
R. Gossage,
MD
Nashville, Tennessee 19 April 1993 1. Cheng TO. Acronyms Am J Cardiol
of major cardiologic trials.
1992:70:1512-1513.
U&278. 4. O’Conell
DJ, MacMahon H, De Mess& TR. Multicentric tracheobronchial and oesophageal granular cell myoblastoma. Thorax 1978;33:596-602. 5. Khanolkar VR Granular cell myoblastoma. Am .I
Relation Between Patent Foramen Ovale and Stroke
Path01 1947;23:721-739.
Svejda J, Horn V. Disseminated granular-cell pseudotumor: so-called metastasizing granular-cell myoblastoma. .I Path01 1958;76:343-348. 7. Kubac G, Doris I, Ondro M, Davey PW. Malignant granular cell myoblaatoma with metastatic cardiac involvement; case report and echocardiogram. Am Heart J 1980; 100~227-229. 6. Ravich A, Stout AP, Ravich RA. Malignant granular cell myoblastoma involving the urinary bladder. Ann Surg 1945;121:361-372. 6. Kreig AF. Malignant granular cell myoblastoma. 6.
Arch Pathol 1962;74:252-256. 10. Mackenzie DH. Malignant granular cell myoblastoma. J Clin Pathol 1967;20:739-742.
il. Usui M, Ishii S, Yamawaki S, Sasaki T, Minami A, Hizawa K. Malignant granular cell hunor of the radial nerve. An autopsy observation with electron microscopic and tissue culture studies. Cancer 1977; 39:1547-1555.
12. Steffelaar JW, Nap M, Ha&t UJGM. Malignant granular cell tumor. Am J Sur-g Path01 1982;6:665-672.
Lytic Lament
A recent letter to The American Journal of Cardiology provided a prodigious list of acronyms for major clinical trials in cardiology.1 Although incomplete, the list contained over 200 entries! It is unclear to me whether the authors meant to provide a service or humor, but I wish to stray to the lighter side. I was recently asked to give a talk on thrombolysis in acute coronary ischemia at
In their article on the relation between patent foramen ovale (PFO) and unexplained stroke, Van Camp et al’ conclude that early and massive passage of contrast in the left atrium through a PFO is a possible mechanism for stroke. However, 38% of the patients in the stroke group and 25% of the patients in the control group had atrial fibrillation which, by itself, is a major risk factor for stroke.2 They should have excluded patients with atria1 fibrillation in both groups before analyzing the data. If, after exclusion of the 18 patients with atrial fibrillation, the remaining patients show a signilicantly higher incidence of abnormal PFO morphology with early and massive passage of contrast, only then is their conclusion regarding the relation between PFO and stroke valid. Anil
K. Mukeriee.
West Roxbury
Polymorphous Ventricular Tachycardia Early After Acute Myocardial Infarction
The article by Bimbaum and colleagues’ describing polymorphous ventricular tachycardia early after acute myocardial infarction pointed out some important aspects of this condition. However, no mention was made about the role of magnesium in the etiology or treatment of the patients described in that report. Polymorphous ventricular tachycardia in this setting has been reported to respond to magnesium supplementation when other antiarrhythmic drugs failed to stabilize the cardiac rhythm.2 Polymorphous ventricular tachycardia in other clinical settings has also been shown to be associated with magnesium deficiency and respond to intravenous infusion of magnesium.3~4 Magnesium is predominantly an intracellular cation5 with little correlation being found between the measured serum concentration and the intracellular concentration.c8 A role magnesium plays in metabolism is that of a regulator of other ions; this action occurs within the cell at the molecular level and on the cell membrane.9 There is a particularly close relation between intracellular magnesium and potassium.1° The antiarrhythmic or membrane-stabilizing effect of magnesium may be related to its ability to regulate internal potassium homeostasis. l1 Because the serum magnesium concentration does not give an accurate assessment of the magnesium status of a patient, empiric use of magnesium supplementation should be considered in settings known to be associated with magnesium depletion.12 Magnesium is well tolerated when given intravenously, particularly when renal function is not impaired, is effective in a variety of settings, is readily available and is inexpensive. Richard
A. Reinhart,
Marsh6eld,
MD
Mass&h&etis 13 May 1993
MD
Wisconsin 18 May 1993
596598. 2. Petersen
1. Bimbaum Y, Sclarovsky S, Ben-Ami R, Rechavia E, Strasberg B, Kusniec J, Mager A, Sulkes J. Polymorphous ventricular tachycardia early after acute myocardial infarction. Am J Cardiol 1993;71:745-750. 2. Friday BA, Reinhart R4. Magnesium metabolism: a case report and literature review. Crit Care Nurse
1990;819.
3. Ramee SR, White CJ, Svinzuich JT, Watson TD,
1. Van Camp GV, Schulze D, Cosyns B, Vanden-
bossche J-L. Relation between patent foramen ovale and unexplained stroke. Am J Cardiol 1993;71: P. Risk factors for thromboembolic complications in chronic atria1 fibrillation. Arch Intern Med
1991;11:62-72.
READERS COMMENTS 863
Fox RF. Torsades de pointes and magnesium de& ciency. Am Heart J 1985;109:1@-166. 4. Tzivoni D, Keren A, Cohen AM. Magnesium therapy for tormdes de pointes. Am J Cardiol 1984,53: 528-530. 5. Reinlxut RA. Magnesium metabolism: a review with special reference to the relationship between intracellular content and senxn levels. Arch Intern Med 1988;148:2415-2420. 6. Reinhart RA, Marx Jr JJ, Haas RG, Desbiens NA. Inkw.llular magnesium of mononuclear cells from venous blood of clinically healthy subjects. Clin Chim Acta 1987;167:187-195. 7. Reinhart RA, Marx Jr JJ, Broste SK, Haas RG. Myocardial magnesium: relation to laboratory and clinical variables in patients undergoing cardiac surgery. J Am Coil Cardiol 1991;17:651-656, 8. Reinhart RA, Fananapazir L, Cannon Ill RO, Hosseini JM, Elin RJ. Effect of intravenous magnesium sulfate. on blood magnesium parameters. Mqnes Trace Elem 1990;9:191-197. 9. Reinhart RA. Clinical correlates of the molecular and cellular actions of magnesium on the caxliovascular system. Am Heart J 1991;121:1513-1521. 10. Reinhart RA, Broste SK, Spencer S, Marx Jr JJ, Haas RG, Rae P. Relation between magnesium and potassium concentrations in myocardium, skeletal muscle, and mononuclear blocd cells. Clin Chem 1992~38: 2444-2448. 11. white RE, Hartzell HC. Magnesium ion in cardiac function: regulator of ion channels and second messengers. Biochem Phmmacol 1989;38:859-867. 12. Reinbart RA. Magnesium deficiency: recognition and treatment in the emergency medicine setting. Am J Emerg Med 1992;10:78-83.
Prognostic Significance and the Role of DualChamber Pacing in Atrioventricular Delay in Idiopathic Dilated Cardiomyopathy
I read the report by Schoeller et al,’ which described lirst- or second-degree atrioventricular (AV) block as an independent risk factor in patients with idiopathic dilated
864
cardiomyopathy @DC). Their report has added rational data for the development of dual-chamber pacemaker therapy in patients with IDC, which was lirst used by Hochleitner et al2 and mysehT3 A subsequent report by Hochleitner et al4 described improved survival in IDC patients with dual-chamber pacing. It is expected that dual-chamber pacing would lead to a better clinical outcome in many IDC patients with AV delay. The exact mechanism(s) by which dual-chamber pacing improves the compromised hemodynamics in patients with IDC is still unclear, but my previous experience3 has shown that optimal AV setting using dual-chamber pacing can improve left ventricular function by producing an increase in left ventricular filling, thus promoting the use of the Frank-Starling mechanism in IDC patients with lirst-degree AV block. Elimination of the AV valve regurgitation by dual-chamber pacing with a short AV interval should also be considered.5 Unexpected cardisc events due to further progression of AV block would be preventable by the placement of a dualchamber pacemaker in IDC patients with first- or second-degree AV block. The beneficial effect of padrenergic-blocking therapy in IDC has been con6rmed,6 but the presence of AV delay would compromise this therapy. Implantation of a dual-chamber pacemaker would not
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 72
OCTOBER 1,1993
only improve cardiac function in itself, but also facilitate safe p-adrenergic-blocking therapy. Thus, it is expected that dual-chamber pacing would improve the prognosis of lDC patients with lirst- or second-degree AV b1ock.l Given the relatively frequent manifestation of lirst- or second-degree AV delay and its prognostic significance in IDC,’ systematic study should be done to determine the indications for dual-chamber pacing in patients with IDC. Hajime
Kataoka, MD Saiki-city, Japan 20 April
1993
1. Schoeller R, Andresen D, But&x P, Oezcelik K, Vey G, Scbroder. First- or second-degree &oventricular block as a risk factor in idiopathic dilated cardiomyopathy. Am J Cardiol 1993;71:720-726. 2. Hochleitner M, H&tnagl H, Ng CK, Hijrtnagl H, Gschnitzer F, Zechmann W. Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. Am J Cardiol 1990;66: 1cm--m? 3. Kataoka H. Hemodynamic effect of physiological dual chamber pacing in a patient with end-stage dilated cardiomyopathy: a case report. PACE 1991;14: A,”
a”*.
133~435.
4. Hochleitner M, Htirtnagl H, Hiilblagl H, Fridrich L, Gscbnitzer F. Long-term efficacy of physiologic dual-chamber pacing in the treatment of end-stage idiopathic dilated cardiomyopathy. Am J Cardiol1992; 70:132&1325. 5. Brecker SJD, Xiao HB, Sparrow J, Gibson DG. Effects of dual-chamber pacing with short ahioventricular delay in dilated cardiomyopathy. Lancet 1992;340:1308-1312. 6. Waagstein F, Caidahl K, Wall&in I, Be@ CH, Hjalmarson A. Long-term p-blockade in dilated cardiomyopathy: effects of short- and long-term metopro101 treatment followed by withdrawal and readministration of metoprolol. Circulation 1989;80: 551-563.