AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Background

Right ventricular infarction was first recognized in a subgroup of patients with inferior wall myocardial infarctions who demonstrated right ventricular failure and elevated right ventricular filling pressures despite relatively normal left ventricular filling pressures. Increasing recognition of right ventricular infarction, either in association with left ventricular infarction or as an isolated event, emphasizes the clinical significance of the right ventricle to total cardiac function.

Interest in recognizing right ventricular infarction noninvasively has grown because of the therapeutic implications of distinguishing patients with right ventricular dysfunction from those with the more usual clinical presentation of left ventricular dysfunction. Patients with right ventricular infarctions associated with inferior infarctions have much higher rates of significant hypotension, bradycardia requiring pacing support, and in-hospital mortality than isolated inferior infarctions (Chockalingam, 2005).

Pathophysiology

The right ventricle is a thin-walled chamber that functions at low oxygen demands and pressure. It is perfused throughout the cardiac cycle in both systole and diastole, and its ability to extract oxygen is increased during hemodynamic stress. All of these factors make the right ventricle less susceptible to infarction than the left ventricle.

The posterior descending branch of the right coronary artery usually supplies the inferior and posterior walls of the right ventricle. The marginal branches of the right coronary artery supply the lateral wall of the right ventricle. The anterior wall of the right ventricle has a dual blood supply: the conus branch of the right coronary artery and the moderator branch artery, which courses from the left anterior descending artery (Forman et al, 1984).

Interestingly, right ventricular infarction noted at necropsy usually involves the posterior septum and posterior wall rather than the right free wall. The relative sparing of the right ventricular anterior wall apparently arises from a high degree of collateralization. This collateral blood flow is thought to be derived from the thebesian veins and diffusion of oxygen directly from the ventricular cavity. A direct correlation exists between the anatomic site of right coronary artery occlusion and the extent of right ventricular infarction. Studies have demonstrated that more proximal right coronary artery occlusions result in larger right ventricular infarctions (Garty et al, 1984). On occasion, the right ventricle can be subjected to infarction from occlusion of the left circumflex coronary artery (Giannitsis et al, 1997).

Because the right ventricle is considered a low-pressure volume pump, its contractility is highly dependent on diastolic pressure. Hence, when contractility and associated diastolic dysfunction are impaired attendant to right ventricular infarction, the right ventricular diastolic pressure increases substantially and systolic pressure decreases. In such a scenario, concomitant left ventricular dysfunction, with increase in right ventricular afterload, is possible. In such a setting, right ventricular output can decrease dramatically, and the only driving force remaining is elevated right atrial pressure. In such a circumstance, the right ventricle serves as a poorly functioning conduit between the right atrium and the pulmonary artery.

Elevation of right atrial pressure secondary to right ventricular infarction has been noted to serve as a stimulus for secretion of atrial natriuretic factor. Increased levels of this polypeptide can be detrimental to normal left ventricular filling pressures. This occurs by virtue of the potent vasodilating, natriuretic, diuretic, and aldosterone-inhibiting properties of atrial natriuretic factor. Inappropriately elevated levels of atrial natriuretic factor may worsen the clinical syndrome of right ventricular infarction (Haupt et al, 1983). The potential hemodynamic derangements associated with right ventricular infarction render the afflicted patient unusually sensitive to diminished preload (ie, volume) and loss of atrioventricular synchrony. These two circumstances can result in a severe decrease in right and, secondarily, left, ventricular output (Hirsowitz et al, 1984; Hurst, 1998; Iqbal and Liebson, 1981).

Early thrombolysis or mechanical reperfusion of an occluded coronary artery resulting in right ventricular infarction is associated with prompt reduction in right atrial pressure. This is extremely important because persistently elevated right atrial pressure has been associated with increased in-hospital mortality rate when associated with myocardial infarction. The extent of right ventricular infarction varies greatly and is dependent on the site of occlusion of the right ventricular arterial supply. If occlusion occurs before the right ventricular marginal branches, and collateral blood flow from the left anterior descending coronary artery is absent, then the size of infarction generally is greater. Extent of infarction depends somewhat on flow through the thebesian veins (Kinn et al, 1995). In general, any major reduction in blood supply to the right ventricular free wall portends an adverse prognosis in association with this disorder.

Frequency

United States

Isolated infarction of the right ventricle is extremely rare; right ventricular infarction usually is noted in association with inferior wall myocardial infarction. The incidence of right ventricular infarction in such cases ranges from 10-50%, depending on the series (Andersen, Nielsen, Falk et al, 1989).

The frequency of right ventricular infarction, which can be detected by right-sided precordial leads, in association with non–ST-segment elevation or non–Q-wave myocardial infarction is not known and currently is being investigated. Although right ventricular infarction is clinically evident in a sizable number of cases, the incidence is considerably less than that found at autopsy (Andersen, 1987; Andersen, Nielsen, Lund, 1989; Bates, 1997; Birnbaum et al, 1999). A major reason for the discrepancy is the difficulty in establishing the presence of right ventricular infarction in living subjects. Additionally, right ventricular dysfunction and stunning frequently is of a transient nature, such that estimation of its true incidence is even more difficult.

Criteria have been set forth to diagnose right ventricular infarction; even when strictly employed, however, the criteria lead to underestimation of the true incidence of right ventricular infarction (Braat et al, 1984; Braat et al, 1983; Elkayam et al, 1979).

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

History

• Although right ventricular infarction occurs in more than 30% of patients with inferior posterior left ventricular myocardial infarction, hemodynamically significant right ventricular infarction occurs in less than 10% of these patients (Lisbona et al, 1983; Martin et al, 1989).
• A right ventricular infarct should be considered in all patients who present with an acute inferior wall myocardial infarction, especially in the setting of a low cardiac output.
• Patients may describe symptoms consistent with hypotension.
• A subtle clue to the presence of hemodynamically significant right ventricular infarction is a marked sensitivity to preload-reducing agents such as nitrates, morphine, or diuretics (Mittal, 1994).
• Other presentations include high-grade atrioventricular block, tricuspid regurgitation, cardiogenic shock, right ventricular free wall rupture, and cardiac tamponade.
• Should a patient with right ventricular infarction experience unexplained hypoxia despite administration of 100% oxygen, right-to-left shunting at the atrial level in the presence of right ventricular failure and increased right atrial pressure must be considered (Nader et al, 1981; Pfisterer et al, 1990). Despite its rarity, this complication of right ventricular infarction must always be considered when a patient with myocardial infarction is thought to have hypoxia secondary to clinically silent pulmonary emboli. The mechanism for right-to-left shunting in the absence of increased pulmonary arterial pressure resides in patency of the foramen ovale in association with poor right ventricular compliance and increased right atrial filling pressures.
• Patients with extensive right ventricular necrosis are at risk for right ventricular catheter–related perforation, and passage of a floating balloon catheter or pacemaker must always be performed with great care in such a setting.

Physical

• The classic clinical triad of right ventricular infarction includes distended neck veins, clear lung fields, and hypotension (Mavric et al, 1990).
• Infrequent clinical manifestations include right ventricular third and fourth heart sounds, which are typically audible at the left lower sternal border and increase with inspiration.
• On hemodynamic monitoring, disproportionate elevation of right-sided filling pressures compared with left-sided hemodynamics represents the hallmark of right ventricular infarction.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Imaging Studies

• In the appropriate clinical setting, a diagnosis of right ventricular infarction can be made using noninvasive techniques, or the patient may require right ventricular catheterization and hemodynamic monitoring.
• Echocardiography is useful as a modality to rule out pericardial disease and tamponade, which are the major differential diagnoses in the setting of a right ventricular infarction.
• • Right ventricular dilatation, abnormal right ventricular wall motion, paradoxical motion of the interventricular septum, and tricuspid regurgitation are echocardiographic features of right ventricular infarction.
  • As might be expected, tricuspid regurgitation in this setting is detected more frequently by ultrasound than by auscultation of a tricuspid regurgitation murmur.
  • Echocardiogram can detect shunting through a patent foramen ovale.
  • Echocardiogram has an 82% sensitivity and 93% specificity in detecting right ventricular infarction when right ventricular scintigraphy is used as the comparative standard (Singhal et al, 1984).
  • In the vast majority of patients with right ventricular infarction, the wall motion abnormalities initially manifest on echocardiography reverse within 3 months (Strauss et al, 1980).
  • The recent utilization of tissue Doppler in echocardiography has also increased, providing another means to detect right ventricular infarction. A decrease in the systolic velocity at the tricuspid annulus not only allows for diagnosis of right ventricular infarction but also suggests worse mortality outcome (Hisham, 2005).
  • Another echocardiographically obtained value that can aid in diagnosis of right ventricular infarction is the myocardial performance index (MPI). MPI is derived from the sum of the isovolumic relaxation and contraction time divided by the ejection fraction. An abnormally elevated MPI of > 0.30 suggests the presence of a right ventricular infarction (Chockalingam, 2004).
• Gated equilibrium radionuclide angiography and technetium 99m pyrophosphate scintigraphy are useful in diagnosing right ventricular infarction noninvasively (Sugimoto et al, 1996). In the case of radionuclide angiography, the right ventricle is demonstrated to be enlarged and poorly contractile, with a reduced ejection fraction. When technetium 99m pyrophosphate is employed, the right ventricular free wall is "hot," indicating significant infarction.

Other Tests

• Electrocardiography
• • All patients with inferior wall myocardial infarction should have a right-sided ECG. ST-segment elevation in lead V4R is the single most powerful predictor of right ventricular involvement, identifying a high-risk subset of patients in the setting of inferior wall myocardial infarction (Robalino et al, 1990). The ST-segment elevation is transient, disappearing in less than 10 hours following its onset in half of patients. The following table demonstrates the sensitivity and specificity of more than 1 mm of ST-segment elevation in V₁, V₃R, and V₄R (Roth et al, 1990).

    Sensitivity and Specificity of more than 1 mm of ST-Segment Elevation in V₁, V₃R, and V₄R

    Leads	Sensitivity (%)	Specificity (%)
    V1	28	92
    V3R	69	97
    V4R	93	95

  • Isolated right ventricular infarct is extremely rare and may be interpreted erroneously as left ventricular anteroseptal infarction on ECG because of ST-segment elevation in leads V₁-V₄ (Schuler et al, 1984; Sharpe et al, 1978). Some have suggested that the differential diagnosis between the 2 abnormalities can be distinguished by using vectorial analysis. The mean ST-segment vector in right ventricular infarction usually is directed anteriorly and to the right (>100°).
  • In an anteroseptal left ventricular infarct, the mean ST-segment vector is oriented leftward between -30° and -90° thus, analysis of the frontal and horizontal plane axis of the mean ST-segment vector can distinguish electrocardiographically between myocardial infarction at these 2 sites (Silverman, 1982). There has also been some discussion about right ventricular infarctions giving rise to an epsilon wave. However, because of the low voltage of this wave, low sensitivity, and low specificity, thiselectrocardiographic feature is of little value in daily practice (Zorio, 2005).
• Hemodynamic monitoring
• • Disproportionate elevation of right-sided filling pressures when compared with left-sided hemodynamics represents the hallmark of right ventricular infarction.
  • Accepted hemodynamic criteria for right ventricular infarction include right atrial pressure greater than 10 mm Hg, right atrial–to–pulmonary capillary wedge pressure ratio greater than 0.8, or right atrial pressure within 5 mm Hg of the pulmonary capillary wedge pressure. These values may manifest only after volume loading (Sugiura et al, 1994).
  • In the setting of right ventricular infarction, pulmonary capillary wedge pressure may be misleading and not accurately reflect left ventricular end-diastolic volume but rather impaired left ventricular filling due to bowing of the interventricular septum into the left ventricle (Tan et al, 1997).
  • Other interesting hemodynamic features of right ventricular infarction include the following:
    • Prominent "y" descent of the right atrial pressure
    • Increase in venous or right atrial pressure with inspiration (ie, Kussmaul sign)
    • Exaggeration of the normal inspiratory decline in systemic arterial pressure (ie, pulsus paradoxus)
    • Elevation of right ventricular filling pressure with early diastolic dip and plateau
• Some of these hemodynamic derangements superficially resemble those of restrictive or constrictive physiology.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Medical Care

Right ventricular infarction should always be considered in any patient who has inferior wall myocardial infarction and associated hypotension, especially in the absence of rales. This entity is preeminently suitable for therapy as outlined in this section. The objectives in managing right ventricular infarctions are maintaining right ventricular preload, maintaining inotropic support while at the same time reducing afterload, and achieving early reperfusion.

Recently, the use of inhaled nitric oxide has been of interest to treat patients with right ventricular infarctions complicated by cardiogenic shock. The principle behind this experimental treatment is that by specifically decreasing pulmonary vascular resistance without compromising systemic vascular resistance, the filling of the left ventricle can be improved with a resultant improvement of systemic cardiac output. Utilization of inhaled nitric oxide in this setting has been associated with rapid improvement of hemodynamics (Inglessis, 2004).

• Maintenance of right ventricular preload: The initial step in managing hypotension should consist of volume loading with 1-2 L of isotonic sodium chloride solution over a 1- to 2-hour period. If hypotension persists, consider hemodynamic monitoring with a pulmonary artery catheter, keeping in mind the following admonitions concerning right ventricular perforation. Patients with extensive right ventricular necrosis are at risk for right ventricular catheter–related perforation, and passage of a floating balloon catheter or pacemaker must always be performed with great care in such a setting.
• Maintenance of inotropic support and afterload reduction: If volume loading does not correct hypotension and restore cardiac output, then inotropic support with dobutamine may be attempted. However, owing to the unpredictable hemodynamic responses that may occur with dobutamine, particularly during hypotension associated with right ventricular infarction, this agent should be used with caution. Concomitant left ventricular dysfunction may necessitate use of an intraaortic balloon pump and/or nitroprusside infusion for afterload reduction. Because of the critical roles of atrioventricular synchrony and atrial transport in maintaining cardiac output, atrioventricular sequential pacing is the modality of choice when a pacemaker is required (Tobinick et al, 1978).
• Achieving early reperfusion: Current available evidence indicates that patients presenting within 6 hours of onset of inferior wall myocardial infarction with right ventricular involvement diagnosed by ECG or other noninvasive criteria have a definite early survival benefit from thrombolytic therapy or coronary angioplasty (Vesterby and Steen, 1984; Yoshino et al, 1998). Scant data exist regarding improvement in patients who present later than 12 hours after onset, and these patients most likely would do well with a conservative management strategy, considering the often spontaneous resolution of right ventricular dysfunction (Zeymer et al, 1998).

Surgical Care

Severe tricuspid regurgitation in the setting of acute right ventricular infarction can be managed with either valve replacement or repair with angioplasty rings, because the incompetent valve may serve as a mechanical impediment to maintenance of adequate cardiac output. Finally, should a patient develop arterial hypoxemia secondary to right-to-left shunting at the atrial level, then an atrial septal defect–occluding device should be considered immediately. However, if for any reason, a delay occurs in placement of the occluding device, inhaled nitric oxide can decrease the right-to-left shunting and increase systemic oxygenation (Inglessis, 2004).

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Cardiovascular agents

Dobutamine is an inotropic agent used to improve right ventricular contractility and maintain cardiac output. Sodium nitroprusside reduces afterload.

Drug Name	Nitroprusside (Nitropress)
Description	Produces vasodilation and increases inotropic activity of heart. At higher doses, may exacerbate myocardial ischemia by increasing heart rate. Infusion rates >10 mcg/kg/min may lead to cyanide toxicity.
Adult Dose	0.3-0.5 mcg/kg/min IV initial infusion; use 0.5 mcg/kg/min increments and titrate to desired effect; average dose is 1-6 mcg/kg/min
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; subaortic stenosis; idiopathic hypertrophic subaortic stenosis; decreased cerebral perfusion; arteriovenous shunt or coarctation of aorta (eg, compensatory hypertension); atrial fibrillation or flutter
Interactions	Other hypotensive agents may have additive effects
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside has ability to lower blood pressure and should be used only in patients with mean arterial pressures >70 mm Hg

Drug Category: Tissue plasminogen activators

These agents bind to fibrin and convert plasminogen to plasmin, which in turn initiates local fibrinolysis with limited systemic proteolysis.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Medical/Legal Pitfalls

• The majority of litigation involving right ventricular infarction, as with myocardial infarction as a whole, involves missing the diagnosis rather than specific errors in treating the condition. In fact, more malpractice awards are for this reason than for any other diagnosis and usually involve emergency physicians, since they are involved in the initial evaluation of the patient seeking treatment for "chest pain." Moreover, claims also arise from not providing appropriate therapy in a timely manner, which has increased in importance because of time-sensitive therapies that have become the standard of care.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

• Andersen HR, Nielsen D, Falk E, et al. Right ventricular infarction: larger enzyme release with posterior than with anterior involvement. Int J Cardiol. Mar 1989;22(3):347-55. [Medline].
• Andersen HR, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol. Dec 1987;10(6):1223-32. [Medline].
• Andersen HR, Nielsen D, Lund O. Prognostic significance of right ventricular infarction diagnosed by ST elevation in right chest leads V3R to V7R. Int J Cardiol. Jun 1989;23(3):349-56. [Medline].
• Bates ER. Revisiting reperfusion therapy in inferior myocardial infarction. J Am Coll Cardiol. Aug 1997;30(2):334-42. [Medline].
• Birnbaum Y, Wagner GS, Barbash GI. Correlation of angiographic findings and right (V1 to V3) versus left (V4 to V6) precordial ST-segment depression in inferior wall acute myocardial infarction. Am J Cardiol. Jan 15 1999;83(2):143-8. [Medline].
• Braat SH, Brugada P, den Dulk K. Value of lead V4R for recognition of the infarct coronary artery in acute inferior myocardial infarction. Am J Cardiol. Jun 1 1984;53(11):1538-41. [Medline].
• Braat SH, Brugada P, de Zwaan C. Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction. Br Heart J. Apr 1983;49(4):368-72. [Medline].
• Chockalingam A, Gnanavelu G, Subramaniam T. Right ventricular myocardial infarction: presentation and acute outcomes. Angiology. Jul-Aug 2005;56(4):371-6.
• Chockalingam A, Gnanavelu G, Alagesan R. Myocardial performance index in evaluation of acute right ventricular myocardial infarction. Echocardiography. Aug 2004;21(6):587-94.
• Dokainish H, Abbey H, Gin K. Usefulness of tissue Doppler imaging in the diagnosis and prognosis of acute right ventricular infarction with inferior wall acute left ventricular infarction. Am J Cardiol. May 1 2005;95(9):1039-42.
• Elkayam U, Halprin SL, Frishman W. Echocardiographic findings in cardiogenic shock due to right ventricular myocardial infarction. Cathet Cardiovasc Diagn. 1979;5(3):289-94. [Medline].
• Forman MB, Goodin J, Phelan B. Electrocardiographic changes associated with isolated right ventricular infarction. J Am Coll Cardiol. Sep 1984;4(3):640-3. [Medline].
• Freas GC. Medicolegal aspects of acute myocardial infarction. Emerg Med Clin North Am. May 2001;19(2):511-21. [Medline].
• Garty I, Barzilay J, Bloch L. The diagnosis and early complications of right ventricular infarction. Eur J Nucl Med. 1984;9(10):453-60. [Medline].
• Giannitsis E, Potratz J, Wiegand U. Impact of early accelerated dose tissue plasminogen activator on in- hospital patency of the infarcted vessel in patients with acute right ventricular infarction. Heart. Jun 1997;77(6):512-6. [Medline].
• Haupt HM, Hutchins GM, Moore GW. Right ventricular infarction: role of the moderator band artery in determining infarct size. Circulation. Jun 1983;67(6):1268-72. [Medline].
• Hirsowitz GS, Lakier JB, Goldstein S. Right ventricular function evaluated by radionuclide angiography in acute myocardial infarction. Am Heart J. Oct 1984;108(4 Pt 1):949-54. [Medline].
• Hurst JW. Comments about the electrocardiographic signs of right ventricular infarction. Clin Cardiol. Apr 1998;21(4):289-91. [Medline].
• Inglessis I, Shin JT, Lepore JJ. Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock. J Am Coll Cardiol. Aug 18 2004;44(4):793-8.
• Iqbal MZ, Liebson PR. Counterpulsation and dobutamine. Their use in treatment of cardiogenic shock due to right ventricular infarct. Arch Intern Med. Feb 1981;141(2):247-9. [Medline].
• Kinn JW, Ajluni SC, Samyn JG. Rapid hemodynamic improvement after reperfusion during right ventricular infarction. J Am Coll Cardiol. Nov 1 1995;26(5):1230-4. [Medline].
• Lisbona R, Sniderman A, Derbekyan V. Phase and amplitude imaging in the diagnosis of acute right ventricular damage in inferior infarction. Clin Nucl Med. Nov 1983;8(11):517-20. [Medline].
• Martin W, Tweddel A, McGhie I. The evaluation of right ventricular function in acute myocardial infarction by xenon-133. Nucl Med Commun. Jan 1989;10(1):35-43. [Medline].
• Mavric Z, Zaputovic L, Matana A. Prognostic significance of complete atrioventricular block in patients with acute inferior myocardial infarction with and without right ventricular involvement. Am Heart J. Apr 1990;119(4):823-8. [Medline].
• Mittal SR. Isolated right ventricular infarction. Int J Cardiol. Aug 1994;46(1):53-60. [Medline].
• Nader DA, Ceretto WJ, Vieweg WV. Atrial pacing in the management of right ventricular infarction. South Med J. Mar 1981;74(3):362-3. [Medline].
• Pfisterer M, Emmenegger H, Muller-Brand J. Prevalence and extent of right ventricular dysfunction after myocardial infarction--relation to location and extent of infarction and left ventricular function. Int J Cardiol. Sep 1990;28(3):325-32. [Medline].
• Robalino BD, Petrella RW, Jubran FY. Atrial natriuretic factor in patients with right ventricular infarction. J Am Coll Cardiol. Mar 1 1990;15(3):546-53. [Medline].
• Roth A, Miller HI, Kaluski E. Early thrombolytic therapy does not enhance the recovery of the right ventricle in patients with acute inferior myocardial infarction and predominant right ventricular involvement. Cardiology. 1990;77(1):40-9. [Medline].
• Saw J, Davies C, Fung A. Value of ST elevation in lead III greater than lead II in inferior wall acute myocardial infarction for predicting in-hospital mortality and diagnosing right ventricular infarction. Am J Cardiol. Feb 15 2001;87(4):448-50, A6. [Medline].
• Schuler G, Hofmann M, Schwarz F. Effect of successful thrombolytic therapy on right ventricular function in acute inferior wall myocardial infarction. Am J Cardiol. Nov 1 1984;54(8):951-7. [Medline].
• Sharpe DN, Botvinick EH, Shames DM. The noninvasive diagnosis of right ventricular infarction. Circulation. Mar 1978;57(3):483-90. [Medline].
• Silverman BD, Carabajal NR, Chorches MA. Tricuspid regurgitation and acute myocardial infarction. Arch Intern Med. Jul 1982;142(7):1394-5. [Medline].
• Singhal AM, Ilangovan S, Mehta S. Isolated right ventricular infarction followed by posterior left ventricular infarction after a few days. Acta Cardiol. 1984;39(4):307-12. [Medline].
• Strauss HD, Sobel BE, Roberts R. The influence of occult right ventricular infarction on enzymatically estimated infarct size, hemodynamics and prognosis. Circulation. Sep 1980;62(3):503-8. [Medline].
• Sugimoto T, Ogawa K, Asada T. Surgical treatment of ventricular septal perforation with right ventricular infarction. J Cardiovasc Surg (Torino). Feb 1996;37(1):71-4. [Medline].
• Sugiura T, Iwasaka T, Shiomi K. Clinical significance of right ventricular dilatation in patients with right ventricular infarction. Coron Artery Dis. Dec 1994;5(12):955-9. [Medline].
• Tan HC, Yeo TC, Lim YT. A case of unusual electrocardiographic presentation of right ventricular myocardial infarction. Ann Acad Med Singapore. Nov 1997;26(6):844-7. [Medline].
• Tobinick E, Schelbert HR, Henning H. Right ventricular ejection fraction in patients with acute anterior and inferior myocardial infarction assessed by radionuclide angiography. Circulation. Jun 1978;57(6):1078-84. [Medline].
• Tsuka Y, Sugiura T, Hatada K. Clinical significance of ST-segment elevation in lead V1 in patients with acute inferior wall Q-wave myocardial infarction. Am Heart J. Apr 2001;141(4):615-20. [Medline].
• Vesterby A, Steen M. Isolated right ventricular myocardial infarction. A case report. Acta Med Scand. 1984;216(2):233-5. [Medline].
• Yoshino H, Udagawa H, Shimizu H. ST-segment elevation in right precordial leads implies depressed right ventricular function after acute inferior myocardial infarction. Am Heart J. Apr 1998;135(4):689-95. [Medline].
• Zehender M, Kasper W, Kauder E. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med. Apr 8 1993;328(14):981-8. [Medline].
• Zeymer U, Neuhaus KL, Wegscheider K. Effects of thrombolytic therapy in acute inferior myocardial infarction with or without right ventricular involvement. HIT-4 Trial Group. Hirudin for Improvement of Thrombolysis. J Am Coll Cardiol. Oct 1998;32(4):876-81. [Medline].
• Zorio E, Arnau MA, Rueda J. The presence of epsilon waves in a patient with acute right ventricular infarction. Pacing Clin Electrophysiol. Mar 2005;28(3):245-7.

Article Last Updated: Jun 29, 2006